Invited Speakers  

Invited Speakers

 Invited speakers (Arranged vertically in alphabetical order by their last name)  

More information on Invited Speakers for INRS2018 will be updated soon.

   Keynote Speech 

 Thomas C. Südhof, M.D. 
 Nobel Prize in Physiology or Medicine, Nobel Foundation (2013)
 Avram Goldstein Professor in The School of Medicine and
 Professor, By Courtesy, of Neurology and of Psychiatry and Behavioral Sciences

 The Department of Molecular and Cellular Physiology
 Stanford University
 Stanford, CA, USA

 

 Bio
Thomas Christian Südhof was born in Göttingen, Germany, on Dec. 22 in 1955, obtained his M.D. and doctoral degrees from the University of Göttingen in 1982. He performed his doctoral thesis work at the Max-Planck-Institut für biophysikalische Chemie in Göttingen with Prof. Victor P. Whittaker on the biophysical structure of secretory granules. From 1983-1986, Südhof trained as a postdoctoral fellow with Drs. Mike Brown and Joe Goldstein at UT Southwestern in Dallas, TX, and elucidated the structure, expression and cholesterol-dependent regulation of the LDL receptor gene. Südhof began his independent career as an assistant professor at UT Southwestern in 1986. When Südhof started his laboratory, he decided to switch from cholesterol metabolism to neuroscience, and to pursue a molecular characterization of synaptic transmission. His work initially focused on the mechanism of neurotransmitter release which is the first step in synaptic transmission, and whose molecular basis was completely unknown in 1986. Later on, Südhof's work increasingly turned to the analysis of synapse formation and specification, processes that mediate the initial assembly of synapses, regulate their maintenance and elimination, and determine their properties. Südhof served on the faculty of UT Southwestern in Dallas until 2008, and among others was the founding chair of the Department of Neuroscience at that institution. In 2008, Südhof moved to Stanford, and became the Avram Goldstein Professor in the School of Medicine at Stanford University. In addition, Südhof has been an Investigator of the Howard Hughes Medical Institute since 1986.

Academic Appointments
Professor, Molecular & Cellular Physiology
Professor (By courtesy), Neurology & Neurological Sciences
Professor (By courtesy), Psychiatry and Behavioral Sciences
Member, Bio-X
Member, Child Health Research Institute
Member, Stanford Neurosciences Institute
Honors & Awards
Elected member, National Academy of Sciences (2002)
Elected member, Institute of Medicine (2008)
Kavli Prize in Neuroscience, Kavli Foundation (2010)
Elected member, American Academy of Arts and Sciences (2010)
Lasker~DeBakey Basic Medical Research Award, Albert and Mary Lasker Foundation (2013)
Nobel Prize in Physiology or Medicine, Nobel Foundation (2013)

Current Research and Scholarly Interests
Human thought and perception, emotions and actions universally depend on signaling between neurons in the brain. This signalling largely happens at synapses, specialized intercellular junctions formed by pre- and postsynaptic neurons. When stimulated, a presynaptic neuron releases chemical messages called neurotransmitters— that is recognized by a postsynaptic neuron.

For decades, the majority of neuroscientists focused their research on the postsynaptic neuron and its role in learning and memory. But throughout his career, Thomas Südhof has studied the presynaptic neuron. His collective findings have provided much of our current scientific understanding of presynaptic neuron behavior in neurotransmission and synapse formation. His work also has revealed the role of presynaptic neurons in neuropsychiatric illnesses, such as autism or neurodegenerative disorders.
Born in Germany, Südhof obtained a medical degree from the University of Gottingen in 1982. He became familiar with neuroscience when he performed research for his doctoral degree at the Max Planck Institute for Biophysical Chemistry. His thesis dealt with the release of hormones from adrenal cells, a model of neurotransmitter release.
To expand his knowledge of biochemistry and molecular biology, Südhof started to work in 1983 as a postdoctoral fellow at the laboratories of Michael Brown and Joseph Goldstein at the University of Texas Southwestern Medical Center at Dallas. He cloned the gene for the receptor of LDL (the low-density lipoprotein), a particle in the blood that transports cholesterol. Moreover, his work identified the sequences that mediate the regulation of the LDL receptor gene expression by cholesterol.
In 1986, Südhof started his own laboratory at UT Southwestern. He began his inquiry into the presynaptic neuron. At the time, what scientists mainly knew about the presynaptic neuron was that calcium ions stimulate the release of neurotransmitters from membrane-bound sacs called vesicles into the synapse, in a process that takes less than a millisecond.
But much was unknown: What allowed rapid neurotransmitter release? How did release occur at the specific region of the neuron the synapse? How did repeated activity change the presynaptic neuron? How did the pre- and postsynaptic neurons come together at the synapse?
Südhof decided to try to answer these questions. Among the discoveries in his 20 years of research, Südhof revealed how synaptotagmin proteins sense calcium and mediate neurotransmitter release from presynaptic neurons. He also defined the molecules that organize release in space and time at a synapse, such as RIMs and Munc13's, and identified central components of the presynaptic machinery that mediate the fusion of synaptic vesicles containing neurotransmitters with the presynaptic plasma membrane, the process that ultimately causes neurotransmitter release, and that is controlled by synaptotagmins.
Südhof's work also revealed how pre- and postsynaptic proteins form physical connections, permitting neurotransmission. Specifically, he identified proteins on presynaptic neurons, called neurexins, and proteins on the postsynaptic neuron, called neuroligins, that bind to each other at the synapse. There are many types of neurexins and neuroligins. Their variable pairing shapes the wide variability in the types of synapses in the brain. Mutations in these proteins severely impair synapse function in mice, and contribute to the pathogenesis of disease such as autism and schizophrenia in humans.
At present, Südhof's lab attempts to build on these findings in defining the relationship between specific synaptic proteins and information processing in the brain, with its concordant manifestations in behavior. This large-scale project attempts to provide insight both into the mechanisms undelying synaptic communication, and the processes causing human disease.

Selected Recent Publications
[1] Bacaj T, Wu D, Burré J, Malenka RC, Liu X, Südhof TC (2015) Synaptotagmin-1 and -7 Are Redundantly Essential for Maintaining the Capacity of the Readily-Releasable Pool of Synaptic Vesicles. PLoS Biol 13:e1002267.
[2] Pak C, Danko T, Zhang Y, Aoto J, Anderson G, Maxeiner S, Yi F, Wernig M, Südhof TC (2015) Human Neuropsychiatric Disease Modeling using Conditional Deletion Reveals Synaptic Transmission Defects Caused by Heterozygous Mutations in NRXN1. Cell Stem Cell 17:316-328.
[3] Zhang B, Chen LY, Liu X, Maxeiner S, Lee SJ, Gokce O, Südhof TC (2015) Neuroligins Sculpt Cerebellar Purkinje-Cell Circuits by Differential Control of Distinct Classes of Synapses. Neuron 87:781-796.
[4] Anderson GR, Aoto J, Tabuchi K, Földy C, Covy J, Yee AX, Wu D, Lee SJ, Chen L, Malenka RC, Südhof TC (2015) β-Neurexins Control Neural Circuits by Regulating Synaptic Endocannabinoid Signaling. Cell 162:593-606.
[5] Aoto J, Földy C, Ilcus SM, Tabuchi K, Südhof TC (2015) Distinct circuit-dependent functions of presynaptic neurexin-3 at GABAergic and glutamatergic synapses. Nat Neurosci 18:997-1007.


 V. Reggie Edgerton, Ph.D.

 Distinguished Professor, Neurosurgery
 Professor, Integrative Biology and Physiology, Neurobiology
 Vice Chair, Integrative Biology and Physiology
 University of California, Los Angeles
 CA, USA

 

 

Bio
Dr. Edgerton received his Ph.D. in Exercise Physiology from Michigan State University, Masters from University of Iowa and BS from East Carolina University. He is currently the Director of the Neuromuscular Research Laboratory and a Distinguished Professor of the Departments of Integrative Biology and Physiology, Neurobiology and Neurosurgery. He has been teaching and conducting research at UCLA for over 40 years. His research is focused on how the neural networks in the lumbar spinal cord of mammals, including humans, regain control of standing, stepping and voluntary control of fine movements after paralysis, and how can these motor functions be modified by chronically imposing activity-dependent interventions after spinal cord injury.

Research Interests
Two general questions are being studied in my lab. One is, how, and to what extent, does the nervous system control protein expression in skeletal muscle fibers? These studies have shown that although the nervous system has a significant influence on the kind and amount of specific proteins synthesized, there are factors intrinsic to individual fibers that also define these properties. The results show also that the neural influence that is associated with muscle fiber types is probably not mediated via the amount or pattern of activity of the motor units. Whole muscle, single motor units and single muscle fibers are studied physiologically and biochemically. Light and confocal microscopy including quantitative enzyme analyses and immunofluorescent microscopy are some of the experimental methods used to study motor unit plasticity. The principal animal models used are spinal cord injury, spaceflight and surgically induced compensatory hypertrophy. A second, and general question is how the neural networks in the lumbar spinal cord of mammals, including humans, control stepping and how this stepping pattern becomes modified by chronically imposing specific motor tasks on the limbs after complete spinal cord injury. Limb motion, electromyographic and kinetic data are recorded to define locomotor characteristics. These studies have shown that the mammalian spinal cord can learn specific complex motor tasks such as standing and stepping. Studies are conducted with humans with spinal cord injury as well as with laboratory animals. Approach: My lab has a very multidisciplinary and integrative approach to science. It involves techniques to assess the kinetics and kinematics of locomotion, the activation patterns of those motor pools that generate the movement and the segmental and sensory networks that modulate the output of these motor pools. In our experiments we also study cell and tissue properties (nerve and muscle) that are important in generating the behavioral characteristics observed. These analyses consist of enzyme activities of single muscle or neural cells, cell morphology, the kinds of proteins synthesized, the modulations of the mRNA's of specific myonuclei as well as the physiological properties of the nerve and muscle cells. In short, our studies are designed to define the cellular and subcellular features of tissues that form the basis for the properties of specific movements. We use a variety of experimental perturbations of the neuromuscular system in order to understand its adaptive potential and to define the physiological mechanisms that induce these adaptations. Significance: Our studies have a basic, as well as an applied aspect to them. There are many important, but unanswered questions about the plasticity of the neuromuscular system. Since the neural and the muscular systems are the primary systems that are responsible for the functional features of movement control, it is important to understand how they are defined and how they are modulated to become more or less dysfunctional.

Selected Recent Publications
[1] Kim JA, Roy RR, Zhong H, Alaynick WA, Embler E, Jang C, Gomez G, Sonoda T, Evans RM, Edgerton VR (2016) PPARδ preserves a high resistance to fatigue in the mouse medial gastrocnemius after spinal cord transection. Muscle Nerve 53:287-296.
[2] Sayenko DG, Atkinson DA, Dy CJ, Gurley KM, Smith VL, Angeli C, Harkema SJ, Edgerton VR, Gerasimenko YP (2015) Spinal segment-specific transcutaneous stimulation differentially shapes activation pattern among motor pools in humans. J Appl Physiol 118:1364-1374.
[3] García-Alías G, Truong K, Shah PK, Roy RR, Edgerton VR (2015) Plasticity of subcortical pathways promote recovery of skilled hand function in rats after corticospinal and rubrospinal tract injuries. Exp Neurol 266:112-119.
[4] Gerasimenko Y, Gorodnichev R, Puhov A, Moshonkina T, Savochin A, Selionov V, Roy RR, Lu DC, Edgerton VR (2015) Initiation and modulation of locomotor circuitry output with multisite transcutaneous electrical stimulation of the spinal cord in noninjured humans. J Neurophysiol 113:834-842.
[5] Angeli CA, Edgerton VR, Gerasimenko YP, Harkema SJ (2014) Altering spinal cord excitability enables voluntary movements after chronic complete paralysis in humans. Brain 137:1394-1409.


  Plenary Speech 

 Gong Chen, Ph.D.

 Professor of Biology
 Verne M. Willaman Chair in Life Sciences
 Laboratory of In Vivo Reprogramming

 Huck Institutes of Life Sciences
 The Pennsylvania State University
 University Park, PA, USA

 Research Interests
In vivo reprogramming for brain repair
The major goal of our research is to develop innovative technologies for brain repair using our newly established in vivo cell conversion technology (Guo et al., Cell Stem Cell, BEST of 2014). Reactive gliosis is a common pathological hallmark after brain injury or diseases. Currently there is no method available to reverse glial scar back to normal neural tissue. We have developed a novel technology to convert reactive glial cells, induced by brain injury or Alzheimer's disease, directly into functional neurons in mouse brain in vivo. This is achieved by expressing a single neural transcription factor NeuroD1 in glial cells. We further demonstrated that human astrocytes in culture can be directly converted into functional neurons by a cocktail of small molecules (Zhang et al., Cell Stem Cell, 2015), suggesting that our new technology may potentially benefit millions of patients worldwide.  Our in vivo cell conversion technology may have broad applications in neural repair after stroke, traumatic brain injury, spinal cord injury, Alzheimer's disease, Parkinson's disease, Huntington's disease, ALS, and glioma. We are currently developing both gene therapy and drug therapy for brain repair. 

Selected Recent Publications
[1] Li H, Chen G (2016) In Vivo Reprogramming for CNS Repair: Regenerating Neurons from Endogenous Glial Cells. Neuron 91:728-738.
[2] Tang X, Kim J, Zhou L, Wengert E, Zhang L, Wu Z, Carromeu C, Muotri AR, Marchetto MC, Gage FH, Chen G (2016) KCC2 rescues functional deficits in human neurons derived from patients with Rett syndrome. Proc Natl Acad Sci U S A 113:751-756.
[3] Zhang L, Yin JC, Yeh H, Ma NX, Lee G, Chen XA, Wang Y, Lin L, Chen L, Jin P, Wu GY, Chen G (2015) Small Molecules Efficiently Reprogram Human Astroglial Cells into Functional Neurons. Cell Stem Cell 17:735-747.
[4] Guo Z, Zhang L, Wu Z, Chen Y, Wang F, Chen G (2014) In vivo direct reprogramming of reactive glial cells into functional neurons after brain injury and in an Alzheimer's disease model. Cell Stem Cell 14:188-202.
[5] Wu Z, Guo Z, Gearing M, Chen G (2014) Tonic inhibition in dentate gyrus impairs long-term potentiation and memory in an Alzheimer's disease model. Nat Commun 5:4159.


 

 Le-Ping Cheng, Ph.D.
 Investigator
 Laboratory of Neural Development and Reprogramming
 Shanghai Institutes for Biological Sciences
 Chinese Academy of Sciences (CAS), China

 

 

Research Interests
1. Transcriptional control of neuronal cell fates in the developing spinal cord
The dorsal horn of the spinal cord is an integrative center that transmits and processes diverse somatosensory information. The neurons in the dorsal spinal cord can be grouped into excitatory and inhibitory neurons that use glutamate and GABA/glycine as their fast transmitters, respectively. Diversity of dorsal horn neurons is also indicated by the restricted expression of peptides in distinct subpopulations. We have found that several transcription factors play important roles in determining the acquisition of transmitter phenotypes, the expression of transmitter and peptide receptors, and dorsal horn laminae III/IV neurons in the developing dorsal spinal cord.
 
2. Conversion of astrocytes into functional neurons in vitro and in vivo
Many transcription factors and chromatin-modifying processes play important roles in controlling the stability of the differentiated cellular identity. However, studies of induced pluripotent stem cells (iPSCs) demonstrated that differentiated cells are not irreversibly locked in their mature identity and can be de-differentiated by overexpression of selective transcription factors. More findings that defined transcription factors can directly convert fibroblasts and glial cells to functional neurons further demonstrate the feasibility of direct reprogramming of non-neuronal cells directly into neurons. During the past several years, we have found that a single transcription factor Ascl1 can efficiently convert postnatal astrocytes from mouse dorsal midbrain, into functional, synapse-forming neurons in vitro. Moreover, we have that Ascl1 alone can induce astrocyte-to-neuron conversion in the dorsal midbrain, cortex, and striatum in vivo.

Ongoing projects in the laboratory include:
(1) By analyzing the phenotypes of knockout mice, we are interested in studying how transcription factors control neurotransmitter phenotypes in developing spinal cord.
(2) Conversion of astrocytes and fibroblasts into diverse neuronal cell types, including glutamatergic neurons, GABAergic neurons, motor neurons, cholinergic neurons, dopaminergic neurons, serotonergic neurons, and noradrenergic neurons.
(3) Investigating whether the induced neurons have similar properties with that of the target neurons and whether they can be used for neuronal repair in the injured nervous system. 


           

 Adam Ferguson, Ph.D.

 Associate Professor in Residence of Neurological Surgery
 Principal Investigator, Brain and Spinal Injury Center
 University of California, San Francisco, CA, USA

 

 

Background: Our research focuses on mechanisms of recovery after neurological trauma. Injuries to the brain and spinal cord invoke numerous, interacting biological processes that work in concert to determine recovery success. Some of these biological processes have contradictory effects at different phases of recovery. For example, mechanisms of synaptic regulation can contribute to cell death in the early phases of recovery but may promote plasticity and restoration of function at later stages.  Understanding the mechanisms of recovery in the complex microenvironment of the injured central nervous system (CNS) requires large-scale integration of biological information and functional outcomes (i.e., Bioinformatics). Our work uses a combination of laboratory studies and statistical modeling approaches to provide an information-rich picture of the syndrome produced by trauma in translational in vivo models.  The long term goal of this research is to provide system-level therapeutic targets for enhancing recovery of function after brain and spinal injury.
Overarching goal: Understand and harness CNS plasticity to promote recovery of function after brain and spinal cord injury through bench-science and translational computational approaches.
Ongoing Research:
Computational Syndromic Discovery: Development of aggregate databases of basic spinal cord injury and traumatic brain injury research data from multiple research centers to enable sophisticated knowledge-discovery, data-sharing, and multivariate quantification of the complete constellation of changes produced by neurotrauma.
Bench science: Inflammatory modulation of glutamate-receptor metaplasticity and its role in spinal cord learning and recovery of function after neurotrauma. Techniques: biochemistry (quantitative western, qRT-PCR, ELISA), histology (immunohistochemistry, in situ hybridization), quantitative image analysis (robotic microscopy, confocal, deconvolution, image math) and behavioral analysis (locomotor scaling, fine-motor control, learning and memory).
Primary Thematic Area: Neurobiology
Research Summary: CNS Plasticity, Bioinformatics, and Recovery from Injury

Selected Recent Publications
[1] Yue JK, Robinson CK, Burke JF, Winkler EA, Deng H, Cnossen MC, Lingsma HF, Ferguson AR, McAllister TW, Rosand J, Burchard EG, Sorani MD, Sharma S, Nielson JL, Satris GG, Talbott JF, Tarapore PE, Korley FK, Wang KKW, Yuh EL (2017) Apolipoprotein E epsilon 4 (APOE-ε4) genotype is associated with decreased 6-month verbal memory performance after mild traumatic brain injury. Brain Behav 7:e00791.
[2] Yue JK, Ngwenya LB, Upadhyayula PS, Deng H, Winkler EA, Burke JF, Lee YM, Robinson CK, Ferguson AR, Lingsma HF, Cnossen MC, Pirracchio R, Korley FK, Vassar MJ, Yuh EL, Mukherjee P, Gordon WA, Valadka AB, Okonkwo DO, Manley GT (2017) Emergency department blood alcohol level associates with injury factors and six-month outcome after uncomplicated mild traumatic brain injury. J Clin Neurosci 45:293-298.
[3] Bosetti F, Koenig JI, Ayata C, Back SA, Becker K, Broderick JP, Carmichael ST, Cho S, Cipolla MJ, Corbett D, Corriveau RA, Cramer SC, Ferguson AR, Finklestein SP, Ford BD, Furie KL, Hemmen TM, Iadecola C, Jakeman LB, Janis S, et al. Translational Stroke Research: Vision and Opportunities. Stroke 48:2632-2637.
[4] Yue JK, Burke JF, Upadhyayula PS, Winkler EA, Deng H, Robinson CK, Pirracchio R, Suen CG, Sharma S, Ferguson AR, Ngwenya LB, Stein MB, Manley GT, Tarapore PE (2017) Selective Serotonin Reuptake Inhibitors for Treating Neurocognitive and Neuropsychiatric Disorders Following Traumatic Brain Injury: An Evaluation of Current Evidence. Brain Sci 7:E93.
[5] Dhall SS, Haefeli J, Talbott JF, Ferguson AR, Readdy WJ, Bresnahan JC, Beattie MS, Pan JZ, Manley GT, Whetstone WD (2017) Motor Evoked Potentials Correlate With Magnetic Resonance Imaging and Early Recovery After Acute Spinal Cord Injury. Neurosurgery doi:10.1093/neuros/nyx320.


 Karim Fouad, Ph.D.

 Professor, Co-Director, Neuroscience and Mental Health Institute
 Faculty of Rehabilitation Medicine
 University of Alberta, Canada

 

 

 

Research Interests
The overall goal of our research is to promote functional recovery following spinal cord injury.
Functional recovery following injuries of the central nervous system (CNS) is limited because severed axons are unable to regrow. This inability to regenerate is caused by various factors including growth inhibitory factors in the central nervous system and intracellular properties of injured neurons. Nevertheless, moderate recovery following brain or spinal cord injuries occurs. The underlying mechanisms for this recovery lies in the ability of spared and injured CNS circuitries to rearrange, generally termed as plasticity. To promote functional recovery following spinal cord injury we are currently focusing on the following strategies:
a) trying to understand injury induced plasticity and attempting to enhance this naturally occurring repair mechanism,
b) unravel how rehabilitative training promotes plasticity, and what limits training effciay in the chronic setting,
c) Promoting regeneration of lesioned axons by addressing various regeneration restricting factors in combined treatments.

Selected Recent Publications
[1] Torres-Espín A, Forero J, Schmidt EKA, Fouad K, Fenrich KK (2018) A motorized pellet dispenser to deliver high intensity training of the single pellet reaching and grasping task in rats. Behav Brain Res 336:67-76.
[2] May Z, Kumar R, Führmann T, Tam R, Vulic K, Forero J, Lucas-Osma AM, Fenrich K, Assinck P, Lee MJ, Moulson A, Shoichet MS, Tetzlaff W, Biernaskie J, Fouad K (2017) Adult skin-derived precursor Schwann cell grafts form growths in the injured spinal cord of Fischer rats. Biomed Mater doi:10.1088/1748-605X/aa95f8.
[3] Li Y, Lucas-Osma AM, Black S, Bandet MV, Stephens MJ, Vavrek R, Sanelli L, Fenrich KK, Di Narzo AF, Dracheva S, Winship IR, Fouad K, Bennett DJ (2017) Pericytes impair capillary blood flow and motor function after chronic spinal cord injury. Nat Med 23:733-741. 
[4] Wei D, Hurd C, Galleguillos D, Singh J, Fenrich KK, Webber CA, Sipione S, Fouad K (2016) Inhibiting cortical protein kinase A in spinal cord injured rats enhances efficacy of rehabilitative training. Exp Neurol 283:365-374.
[5] Fenrich KK, May Z, Torres-Espín A, Forero J, Bennett DJ, Fouad K (2016) Single pellet grasping following cervical spinal cord injury in adult rat using an automated full-time training robot. Behav Brain Res 299:59-71. 


 Herbert M. Geller, Ph.D

 Director, Office of Education,
 Chief, Laboratory of Developmental Neurobiology,
 Division of Intramural Research National Heart, Lung, and Blood Institute, NIH,
 Bethesda, MD, USA

 

 

Research Topics
Research in the Geller laboratory focuses on understanding the mechanisms that control axonal growth and pathfinding, both during neural development and to stimulate regeneration after injury to the brain or spinal cord.
The development of neurons and the neuronal response to injury are influenced by interactions between neurons and the second major cell type in the nervous system, glia. The predominant glial cells in the central nervous system, astrocytes, normally provide a favorable environment for neurons by promoting neuronal migration and the outgrowth of dendritic and axonal processes during development. However, after injury, astrocytes become reactive and form a major part of the glial scar that forms around the injury site and inhibit regeneration. Dr. Geller is identifying the molecular mechanisms at work under these different conditions. His ultimate goal is to promote neuronal regeneration after injury by preventing these changes in astrocytes, adding permissive molecules to astrocytes, or causing neurons to ignore inhibitory cues.
Dr. Geller's laboratory is evaluating the mechanisms by which astrocytes provide directional cues for neuronal processes, focusing on the behavior of the growth cones at their tips as they encounter molecular boundaries. Molecules secreted into the extracellular matrix by astrocytes may be permissive or inhibitory for growth and guidance.
One class of inhibitory astrocyte-derived guidance molecule in the extracellular matrix is the family of chondroitin sulfate proteoglycans (CSPGs). Sulfation of chondroitin glycosaminoglycan (GAG) chains is essential for many of their functions. Dr. Geller and his colleagues have demonstrated a selective action of GAG chains due to their decoration by sulfate in the 4-position of N-acetyl-galactosamine. Elimination of only a few sulfates in the chain abrogates biological activity. This suggests the existence of a "sulfation code" by which GAG chains signal. Dr. Geller and his colleagues are conducting experiments to determine this sulfation code for 4-sulfation as well as other positions in the GAG chain. In addition, the team is conducting experiments to identify the receptors and signal transduction mechanism that mediate CSPG actions on neurons.
Collaborative studies are focused at understanding how neuronal guidance is affected by physical rather than chemical cues. Together they have demonstrated that neurite outgrowth can be controlled by the stiffness of the substrate, with different neuronal populations responding to different stiffness. Whether stiffness can be used to control directional outgrowth is an area of current investigation. In addition, the laboratory is investigating how physical cues (stiffness and structural confinement of growth) can affect the response of the neurons to CSPGs.

Biography
Herbert Geller graduated with a Ph.D. from Case Western Reserve University in 1970 and was an assistant and fellow in physiology, pathology, and neurology at the University of Rochester School of Medicine and Dentistry from 1970 to 1972. He joined the Department of Pharmacology and Neurology at Robert Wood Johnson Medical School in New Jersey becoming a professor in 1985. Dr. Geller joined the NIH in 2001 and since 2005 has been a mentor in the Biomedical Engineering Summer Internship Program. In 2012, he served as the co-chair of the NIH-FDA Glycoscience Day. Dr. Geller has authored or co-authored more than 100 papers, and he sits on the editorial boards of the International Journal of Developmental Neuroscience and the Journal of Neuroscience Methods. Dr. Geller holds memberships with the Society for Neuroscience, American Association for the Advancement of Science, and American Society for Cell Biology.

Selected Recent Publications
[1] Yi JH, Katagiri Y, Yu P, Lourie J, Bangayan NJ, Symes AJ, Geller HM (2014) Receptor protein tyrosine phosphatase σ binds to neurons in the adult mouse brain. Exp Neurol 255:12-18.
[2] Dickendesher TL, Baldwin KT, Mironova YA, Koriyama Y, Raiker SJ, Askew KL, Wood A, Geoffroy CG, Zheng B, Liepmann CD, Katagiri Y, Benowitz LI, Geller HM, Giger RJ (2012) NgR1 and NgR3 are receptors for chondroitin sulfate proteoglycans. Nat Neurosci 15:703-712.
[3] Koch D, Rosoff WJ, Jiang J, Geller HM, Urbach JS (2012) Strength in the periphery: growth cone biomechanics and substrate rigidity response in peripheral and central nervous system neurons. Biophys J 102:452-460.
[4] Yu P, Agbaegbu C, Malide DA, Wu X, Katagiri Y, Hammer JA, Geller HM (2015) Cooperative interactions of LPPR family members in membrane localization and alteration of cellular morphology. J Cell Sci 128:3210-3222.
[5] Wang H, Katagiri Y, McCann TE, Unsworth E, Goldsmith P, Yu ZX, Tan F, Santiago L, Mills EM, Wang Y, Symes AJ, Geller HM (2008) Chondroitin-4-sulfation negatively regulates axonal guidance and growth. J Cell Sci 121:3083-3091.


 Xiao-song Gu, M.D.

 Member, Chinese Academy of Engineering
 Professor of Neuroscience
 Nantong University
 Key Lab of Neural Regeneration of Jiangsu Province, China

 

 

About the speaker:
Professor Xiaosong Gu, M.D., is Director of Jiangsu Key Laboratory of Neuroregeneration of Nantong University, Honorary President of Chinese Society for Anatomical Sciences (CSAS) and the chief of Regenerative Medicine Branch of CSAS, Vice President of Chinese Society of Biomedical Engineering. Prof. Gu works as the editor-in-chief of Medical Journal of Communications, associate editor-in-chief of Current Stem Cell Research & Therapy, and the editorial board member of Biomaterials, Cell Transplantation: The Regenerative Medicine Journal, Neuroscience Bulletin, and Neural Regeneration Research.
Prof. Gu focuses his research on tissue engineered nerve and the molecular mechanisms underlying neural regeneration. So far, he has published 112 academic articles in SCI-indexed journals such as Nature Communication, Brain, Biomaterials, Nucleic Acids Research, Progress in Neurobiology, Cell Reports, Journal of Cell Science, Nature Cell Biology, and Stem Cell. As one of the main inventors, he has been granted several Chinese and international patents.

Selected Recent Publications
[1] Liu Y, Zhou Q, Wang Y, Luo L, Yang J, Yang L, Liu M, Li Y, Qian T, Zheng Y, Li M, Li J, Gu Y, Han Z, Xu M, Wang Y, Zhu C, Yu B, Yang Y, Ding F, Jiang J, Yang H, Gu X (2015) Gekko japonicus genome reveals evolution of adhesive toe pads and tail regeneration. Nat Commun 6:10033.
[2] Shi H, Gong Y, Qiang L, Li X, Zhang S, Gao J, Li K, Ji X, Tian L, Gu X, Ding F (2016) Derivation of Schwann cell precursors from neural crest cells resident in bone marrow for cell therapy to improve peripheral nerve regeneration. Biomaterials 89:25-37.
[3] Yu B, Zhou S, Yi S, Gu X (2016) The regulatory roles of non-coding RNAs in nerve injury and regeneration. Prog Neurobiol 134:122-139.
[4] Zhang Z, Yu B, Gu Y, Zhou S, Qian T, Wang Y, Ding G, Ding F, Gu X (2016) Fibroblast-derived tenascin-C promotes Schwann cell migration through β1-integrin dependent pathway during peripheral nerve regeneration. Glia 64:374-385.
[5 Li S, Xue C, Yuan Y, Zhang R, Wang Y, Wang Y, Yu B, Liu J, Ding F, Yang Y, Gu X (2015) The transcriptional landscape of dorsal root ganglia after sciatic nerve transection. Sci Rep 5:16888.


 James D. Guest, M.D., Ph.D.

 Clinical Professor, Department of Neurological Surgery
 The Miami Project to Cure Paralysis
 University of Miami
 FL, USA

 

 

Research Interests
Augmented Recovery after SCI; Application of Therapeutic Combinations in Preclinical Studies, and Early Phase Clinical Trials
The current focus of the Guest lab is on the transplantation of autologous glial cells to repair spinal cord injuries. We utilize several types of animal models with an emphasis on solving translational questions related to human clinical application. We also emphasize minimally-invasive surgical lesion-making and transplantation techniques. Sophisticated outcome assessment techniques are used to evaluate transplant effects in both the acute and chronic state of injury. These include kinematic assessment of hand function and gait, electrophysiologic study of conduction across lesion sites, and sensory testing. Other areas of research include studies of human post-mortem spinal cord tissue, intraoperative human spinal cord conduction studies, and research design for human clinical trials.

Selected Recent Publications
[1] Jones LAT, Bryden A, Wheeler TL, Tansey KE, Anderson KD, Beattie MS, Blight A, Curt A, Field-Fote E, Guest JD, Hseih J, Jakeman LB, Kalsi-Ryan S, Krisa L, Lammertse DP, Leiby B, Marino R, Schwab JM, Scivoletto G, Tulsky DS, et al. (2017) Considerations and recommendations for selection and utilization of upper extremity clinical outcome assessments in human spinal cord injury trials. Spinal Cord doi: 10.1038/s41393-017-0015-5. 
[2] Bastidas J, Athauda G, De La Cruz G, Chan WM, Golshani R, Berrocal Y, Henao M, Lalwani A, Mannoji C, Assi M, Otero PA, Khan A, Marcillo AE, Norenberg M, Levi AD, Wood PM, Guest JD, Dietrich WD, Bartlett Bunge M, Pearse DD (2017) Human Schwann cells exhibit long-term cell survival, are not tumorigenic and promote repair when transplanted into the contused spinal cord. Glia 65:1278-1301. 
[3] Anderson KD, Guest JD, Dietrich WD, Bartlett Bunge M, Curiel R, Dididze M, Green BA, Khan A, Pearse DD, Saraf-Lavi E, Widerström-Noga E, Wood P, Levi AD (2017) Safety of Autologous Human Schwann Cell Transplantation in Subacute Thoracic Spinal Cord Injury. J Neurotrauma 34:2950-2963.
[4] Kwon BK, Streijger F, Hill CE, Anderson AJ, Bacon M, Beattie MS, Blesch A, Bradbury EJ, Brown A, Bresnahan JC, Case CC, Colburn RW, David S, Fawcett JW, Ferguson AR, Fischer I, Floyd CL, Gensel JC, Houle JD, Jakeman LB, et al. (2015) Large animal and primate models of spinal cord injury for the testing of novel therapies. Exp Neurol 269:154-168.
[5] Grossman RG, Fehlings MG, Frankowski RF, Burau KD, Chow DS, Tator C, Teng A, Toups EG, Harrop JS, Aarabi B, Shaffrey CI, Johnson MM, Harkema SJ, Boakye M, Guest JD, Wilson JR (2014) A prospective, multicenter, phase I matched-comparison group trial of safety, pharmacokinetics, and preliminary efficacy of riluzole in patients with traumatic spinal cord injury. J Neurotrauma 31:239-255.


 Zhigang He, Ph.D., B.M.

 Professor of Neurology
 Boston Children's Hospital
 F.M. Kirby Neurobiology Center
 Center for Life Science
 Boston, MA 02115, USA

 

 

About Zhigang He
Zhigang He received his PhD from the University of Toronto and was a postdoctoral fellow with Marc Tessier-Lavigne at the University of California, San Francisco. He has the honor of being named a Klingenstein Fellow in Neuroscience, a John Merck Scholar and a McKnight Scholar.
Dr. He is the director of the Boston Children’s Hospital Viral Core, which aims to provide technological resources to academic investigators interested in the development and use of viral based vectors. The Boston Children’s Hospital Viral Core aims to provide technological resources to academic investigators interested in the development and use of viral based vectors. Currently, we offer custom lentiviral vector production, custom AAV vector production with a variety of serotypes and aliquots of in-stock vector. The Viral Core is located on the 13th floor of the Center for Life Science building.

Research Overview
Zhigang He is interested in why lesioned axons cannot regenerate in the adult mammalian central nervous system (CNS). His research has been focused on two potential mechanisms: the inhibitory activity in the adult lesion sites and reduced intrinsic ability associated with mature CNS neurons.
Previous studies indicate that the inhibitory activity is principally associated with components of CNS myelin and molecules in the glial scar at the lesion site. Recent studies from He's laboratory and others suggested that three myelin proteins -- myelin-associated glycoprotein (MAG), Nogo-A and oligodendrocyte myelin glycoprotein (OMgp) -- collectively account for the majority of the inhibitory activity in CNS myelin. The inhibitory activity of MAG, OMgp and the extracellular domain of Nogo-A might be mediated by a receptor complex with a Nogo receptor and at least two co-receptors, p75/TROY and Lingo-1. Blocking such inhibitory activity by genetic and pharmacological approaches could promote local axonal sprouting and reactivate structural plasticity but is not sufficient to allow long-distance axon regeneration.
Our current studies are aimed to define cellular and molecular mechanisms underlying the intrinsic regenerative capacity of mature neurons. He and his colleagues envision two main possibilities for the lack of axon re-growth responses after an injury: (1) the signals carrying information of axotomy fail to reach to the cell body for activating regenerative program; and/or (2) the axonal growth program could not to be reactivated even if the retrograde signals are delivered to the cell bodies. They are addressing these issues by a combination of in vitro and in vivo approaches.

Selected Recent Publications
[1] Lu Y, Belin S, He Z (2014) Signaling regulations of neuronal regenerative ability. Curr Opin Neurobiol 27C:135-142. 
[2] O'Donovan KJ, Ma K, Guo H, Wang C, Sun F, Han SB, Kim H, Wong JK, Charron J, Zou H, Son YJ, He Z, Zhong J (2014) B-RAF kinase drives developmental axon growth and promotes axon regeneration in the injured mature CNS. J Exp Med 211:801-814.
[3] Ho PP, Kanter JL, Johnson AM, Srinagesh HK, Chang EJ, Purdy TM, van Haren K, Wikoff WR, Kind T, Khademi M, Matloff LY, Narayana S, Hur EM, Lindstrom TM, He Z, Fiehn O, Olsson T, Han X, Han MH, Steinman L, Robinson WH (2012) Identification of naturally occurring fatty acids of the myelin sheath that resolve neuroinflammation. Sci Transl Med 4:137ra73.
[4] Jiang L, Qin X, Zhong X, Liu L, Jiang L, Lu Y, Fan L, He Z, Chen Q (2011) Glycine-induced cytoprotection is mediated by ERK1/2 and AKT in renal cells with ATP depletion. Eur J Cell Biol 90:333-341. 
[5] Park KK, Liu K, Hu Y, Kanter JL, He Z (2010) PTEN/mTOR and axon regeneration. Exp Neurol 223:45-50.


  Xiaoming Jin, Ph.D.

 Associate Professor
 Department of Anatomy & Cell Biology
 Stark Neurosciences Research Institute
 Indiana University School of Medicine
 Indianapolis, IN, USA

 

 

Mechanisms of functional recovery and epileptogenesis in traumatic brain injury.
Our lab is interested in (1) organization and plasticity of cortical circuits, and (2) epileptogenesis following traumatic brain injury. These topics are investigated with a variety of techniques at molecular, cellular and circuit levels, including laser scanning photostimulation combined with whole cell patch clamp recording, organotypic brain slice culture, gene gun transfection, time lapse confocal imaging, and molecular biological techniques. The long-term goals of the lab are to develop therapeutic strategies for the prevention and treatment of posttraumatic epilepsy, for improvement of functional recovery in patients with traumatic brain injury.
Current Studies Include:
A) Understanding the roles and regulation of axonal sprouting in posttraumatic epilepsy. Axonal sprouting is considered one of the major pathological changes in different types of epilepsy, including temporal lobe and posttraumatic epilepsies. This regenerative process also provides a structural basis for functional recovery of the cerebral cortex following various brain damages such as stroke and brain trauma. It is critical to find a way to preserve normal axonal regeneration without maladaptive connectivity that contributes to epileptic seizures after injuries. Using organotypic slice culture and acute brain slice preparation, we are currently studying how axonal sprouting occurs in cortical pyramidal neurons following injury, and if it plays an important role in posttraumatic epileptogenesis.  
B) Anatomy and neurophysiology of the cortical circuits. Understanding how different types of cortical neurons are wired into functional circuits is fundamental to deciphering cortical functions and disorders. We use a combination of glutamate uncaging and whole cell patch clamp recording techniques to study the organization of neural circuits in the neocortex, particularly the long-range corticocortical connections between somatosensory and motor cortices.

Selected Recent Publications
[1] Xiong W, Ping X, Ripsch MS, Chavez GSC, Hannon HE, Jiang K, Bao C, Jadhav V, Chen L, Chai Z, Ma C, Wu H, Feng J, Blesch A, White FA, Jin X (2017) Enhancing excitatory activity of somatosensory cortex alleviates neuropathic pain through regulating homeostatic plasticity. Sci Rep 7:12743. 
[2] Wu W, Xiong W, Zhang P, Chen L, Fang J, Shields C, Xu XM, Jin X (2017) Increased threshold of short-latency motor evoked potentials in transgenic mice expressing Channelrhodopsin-2. PLoS One 12:e0178803. 
[3] Xiong WH, Jin X (2012) Optogenetic field potential recording. J Neurosci Methods 210:119-124.
[4] Xiong W, Ping X, Gao J, Jin X (2011) Preparing undercut model of posttraumatic epileptogenesis in rodents. J Vis Exp 55:2840.
[5] Brittain JM, Duarte DB, Wilson SM, Zhu W, Ballard C, Johnson PL, Liu N, Xiong W, Ripsch MS, Wang Y, Fehrenbacher JC, Fitz SD, Khanna M, Park CK, Schmutzler BS, Cheon BM, Due MR, Brustovetsky T, Ashpole NM, Hudmon A, et al. (2011) Suppression of inflammatory and neuropathic pain by uncoupling CRMP-2 from the presynaptic Ca²? channel complex. Nat Med 17:822-829.


 Byung G. Kim, M.D., Ph.D.
 Professor
 Departments of Brain Science
 Department of Neurology, and Neuroscience Graduate Program
 Department of Biomedical Sciences
 Ajou University School of Medicine
 Republic of Korea

 

 

About the speaker:
Dr. Byung Gon Kim received his MD degree in 1993 from Seoul National University School of Medicine. He completed clinical training in adult Neurology in the Department of Neurology, Seoul National University Hospital, and was board-certified in Neurology specialty in 1998. After having fulfilled his military duty for three years, he moved to the Georgetown University Medical Center in the USA for the study of neural repair and received PhD degree in 2005 from the Interdisciplinary Program in Neuroscience, Georgetown University. He has been running his own neuroscience research lab at Ajou University School of Medicine since Sep. 2005. He is also involved in the outpatient clinic in the field of general neurology at Ajou University Hospital. His primary research interest is axonal regeneration and plasticity in CNS injury. His recent work has focused on inflammatory mediators that influence intrinsic capacity of CNS neurons to regenerate axon in CNS injury such as spinal cord trauma and stroke. He is also running diverse research programs including modulation of microenvironment for neural stem cell transplantation and degeneration and regeneration of the white matter in vascular dementia animal model.


Selected Recent Publications
[1] Kwon MJ, Shin HY, Cui Y, Kim H, Thi AH, Choi JY, Kim EY, Hwang DH, Kim BG (2015) CCL2 mediates neuron-macrophage interactions to drive proregenerative macrophage activation following preconditioning injury. J Neurosci 35:15934-15947.
[2] Hwang DH, Shin HY, Kwon MJ, Choi JY, Ryu BY, Kim BG (2014) Survival of neural stem cell grafts in the lesioned spinal cord is enhanced by a combination of treadmill locomotor training via insulin-like growth factor-1 signaling. J Neurosci 34:12788-12800.
[3] Choi JY, Cui Y, Kang YM, Kim JH, Lee SJ, Kim BG (2014) Role of toll-like receptor 2 in ischemic demyelination and oligodendrocyte death. Neurobiol Aging 35:1643-1653.
Shin HY, Kim H, Kwon MJ, Hwang DH, Lee K, Kim BG (2014) Molecular and cellular changes in the lumbar spinal cord following thoracic injury: regulation by treadmill locomotor training. PLoS One 9:e88215.
[4] Kwon MJ, Kim J, Shin H, Jeong SR, Kang YM, Choi JY, Hwang DH, Kim BG (2013) Contribution of macrophages to enhanced regenerative capacity of dorsal root ganglia sensory neurons by conditioning injury. J Neurosci 33:15095-15108.


 Jae K. Lee, Ph.D.
 Associate Professor
 Department of Neurological Surgery
 The Miami Project to Cure Paralysis
 University of Miami
 FL, USA
 
 

 

 

Research Interests:
After traumatic injury to the central nervous system (CNS), such as spinal cord injury or traumatic brain injury, non-CNS cells such as hematogenous immune cells and fibroblasts enter the CNS parenchyma and cause tissue damage.  In response, glial cells attempt to form a protective barrier but during this process, these reactive glial cells (often called the glial scar) create an environment that is not conducive to tissue repair.  The primary goal of our laboratory is to investigate how these CNS and non-CNS cells interact to form the scar in hopes that a better understanding of this complex process will help promote cellular repair and axon regeneration.
Toward this goal, we are currently investigating the molecular and cellular mechanism of glial and fibrotic scar formation after neurological disorders such as spinal cord injury.  A hallmark of many CNS pathology is the presence of hypertrophic reactive astrocytes.  This is especially true in cases of traumatic CNS injuries where a dense network of interweaving hypertrophic reactive astrocytes surround the injury site.  However, another major cellular component of this glial scar is NG2 cells (a.k.a oligodendrocyte progenitor cells or polydendrocytes) that are commonly overlooked.  We are currently investigating the contribution of NG2 cells to glial scar formation
In addition, we are also investigating the role of fibroblasts that invade the injury site after spinal cord injury. Although the glial scar has received a lot of attention, very little is known about the fibrotic scar after CNS injury.  While the traditional view was that fibroblasts originate from the meninges that surround the brain and spinal cord, our findings identified perivascular fibroblasts as a major source of the fibrotic scar after spinal cord injury and that this process is mediated by hematogenous macrophages.  We are currently investigating the role of the fibrotic scar in CNS disorders and the contribution of macrophages to scar formation.

Selected Recent Publications
[1] Zhu Y, Lyapichev K, Lee DH, Motti D, Ferraro NM, Zhang Y, Yahn S, Soderblom C, Zha J, Bethea JR, Spiller KL, Lemmon VP, Lee JK (2017) Macrophage Transcriptional Profile Identifies Lipid Catabolic Pathways That Can Be Therapeutically Targeted after Spinal Cord Injury. J Neurosci 37:2362-2376.
[2] Hong LTA, Kim YM, Park HH, Hwang DH, Cui Y, Lee EM, Yahn S, Lee JK, Song SC, Kim BG (2017) An injectable hydrogel enhances tissue repair after spinal cord injury by promoting extracellular matrix remodeling. Nat Commun 8:533. 
[3] Hackett AR, Lee JK (2016) Understanding the NG2 Glial Scar after Spinal Cord Injury. Front Neurol 7:199. 
[4] Funk LH, Hackett AR, Bunge MB, Lee JK (2016) Tumor necrosis factor superfamily member APRIL contributes to fibrotic scar formation after spinal cord injury. J Neuroinflammation 13:87. 
[5] Zhu Y, Soderblom C, Trojanowsky M, Lee DH, Lee JK (2015) Fibronectin Matrix Assembly after Spinal Cord Injury. J Neurotrauma 32:1158-1167.


  Vance P. Lemmon, Ph.D.

 Program Director | Computational Biology & Bioinformatics
 Walter G. Ross Distinguished Chair in Developmental Neuroscience
 Professor, Department of Neurological Surgery
 Center for Computational Science
 University of Miami
 Miami, FL, USA

 

About the speaker
Vance Lemmon is the program director for CCS’ Computational Biology & Bioinformatics Program. He holds the Walter G. Ross Distinguished Chair in Developmental Neuroscience at the Miami Project to Cure Paralysis and is a Professor of Neurological Surgery at the University of Miami. He also is an associate member of the John P. Hussman Institute for Human Genomics.
Dr. Lemmon joined The Miami Project to Cure Paralysis in 2003. He collaborates with Prof. John Bixby and uses High Content Analysis to screen drug, compound and cDNA libraries for perturbagens that can enhance nerve regeneration after injury to the central nervous system. Recent publications describing this work have appeared in Science magazine (2009, 2011) and the Proceedings of the National Academy of Sciences, PNAS (2102). The LemBix group uses the CCS HPC resources to analyze next generation sequencing data and run support vector machine algorithms on data from kinase inhibitor experiments. The later project is done in collaboration with Stephan Schürer of CCS.

Research overview
High Content Screening and Functional Genomics of the Nervous System
The mass of information available from the various genome projects, together with sophisticated image analysis and laboratory automation has created an opportunity to revolutionize the study of the nervous system. Our laboratory has developed methods to test hundreds of genes in hundreds of thousands of neurons each week and obtain quantitative information about cell morphology and gene expression. This “high throughput” capability allows us to tackle questions about development and regeneration using Systems Biology approaches. The biological problem we have focused on for the past six years has been to uncover genes that promote or prevent axon regeneration.
The Lemmon-Bixby lab has four ongoing projects related to axon regeneration. The first project springs from the fact that neurons in the peripheral nervous system are able to regenerate while neurons in the central nervous system (CNS) are not. By analyzing data from several molecular biological approaches we were able to identify 900 genes that are preferentially expressed in regenerating peripheral neurons; of particular interest is a sub-list of 40 transcription factors (TFs) that are likely to regulate expression of other genes. The top TF has been confirmed to enhance neurite growth when over-expressed in CNS neurons.
Our second project is based on the fact that young CNS neurons have a greater regenerative capacity than old CNS neurons (collaboration with Dr. Jeff Goldberg). We have used DNA microarray data to generate a list of 800 candidate genes. We have tested about 60% of the genes on our list, and have identified 4 TFs that have a robust effect on neurite growth: two enhance growth and two inhibit growth. Interestingly, the two TFs that enhance growth show decreased expression as development proceeds, and the two that inhibit axon growth show increased expression as the animal ages.
The third project is to test effects of overexpression of known signaling proteins (kinases and phosphatases). In this screen we have tested 724 genes, and have found a high percentage with significant effects on neurite growth (about 40 total). The data from this screen is allowing us to begin to build models of neuronal signaling networks underlying axon regeneration. We are also using cheminformatics (collaboration with Stephan Schuerer) to identify chemicals that alter the activity of the interesting signaling molecules.
The fourth project is to screen a chemical compound library to identify compounds that can overcome the regeneration-inhibitory effects of the injured CNS (collaboration with Prof. Young-Tae Chang, , National University of Singapore). We have identified four compounds that enhance axon growth of a variety of neurons in inhibitory environments. One of these has been found to enhance regeneration in an acute spinal cord injury model in vivo.

Selected Recent Publications
[1] Motti D, Blackmore M, Bixby JL, Lemmon VP (2018) High Content Screening of Mammalian Primary Cortical Neurons. Methods Mol Biol 1683:293-304.
[2] Fischer D, Harvey AR, Pernet V, Lemmon VP, Park KK (2017) Optic nerve regeneration in mammals: Regenerated or spared axons? Exp Neurol 296:83-88. 
[3] Motti D, Lerch JK, Danzi MC, Gans JH, Kuo F, Slepak TI, Bixby JL, Lemmon VP (2017) Identification of miRNAs involved in DRG neurite outgrowth and their putative targets. FEBS Lett 591:2091-2105. 
[4] Al-Ali H, Ding Y, Slepak T, Wu W, Sun Y, Martinez Y, Xu XM, Lemmon VP, Bixby JL (2017) The mTOR Substrate S6 Kinase 1 (S6K1) Is a Negative Regulator of Axon Regeneration and a Potential Drug Target for Central Nervous System Injury. J Neurosci 37:7079-7095. 
[5] Gao H, Danzi MC, Choi CS, Taherian M, Dalby-Hansen C, Ellman DG, Madsen PM, Bixby JL, Lemmon VP, Lambertsen KL, Brambilla R (2017) Opposing Functions of Microglial and Macrophagic TNFR2 in the Pathogenesis of Experimental Autoimmune Encephalomyelitis. Cell Rep 18:198-212.


 Xiao-Jiang Li, M.D., Ph.D.
 Distinguished Professor
 Department of Human Genetics
 Emory University School of Medicine
 Atlanta, GA, USA
 Professor, Guangdong-HongKong-Macau Institute of CNS Regeneration (GHMICR),
 Jinan University, Guangzhou, China

 

 

Research Interests
The main interest of the Li Lab is to understand the molecular mechanisms of inherited neurodegeneration caused by a CAG repeat expansion in the disease genes. Currently, we focus on Huntington's disease (HD), an autosomal dominant genetic disease that is characterized by massive neuronal loss in selective brain regions and affects about 5/100,000 people in North America. The HD protein, huntingtin, forms aggregates in neurons, abnormally interacts with other proteins, and eventually kills neurons. However, it is unclear how mutant huntingtin causes selective neurodegeneration and why the clinical symptoms often occur in mid-life in HD.
To address these important issues, we will use a variety of approaches, including genetic manipulation of animal models, molecular and cell biological analysis of protein transport, and biochemical study of protein-protein interactions, to investigate the relationship between gene mutation and disease phenotypes. Specifically, we are currently investigating the effects of mutant proteins on the function of neurons and glia in the brain, gene transcription, and intracellular trafficking. The goal of our studies is to provide mechanistic insight into the pathogenesis of neurodegeneration caused by polyQ expansion and to help develop effective therapeutic strategies.

Selected Recent Publications
[1] Guo J, Cui Y, Liu Q, Yang Y, Li Y, Weng L, Tang B, Jin P, Li XJ, Yang S, Li S (2018) Piperine ameliorates SCA17 neuropathology by reducing ER stress. Mol Neurodegener 13:4. 
[2] Yang S, Yang H, Chang R, Yin P, Yang Y, Yang W, Huang S, Gaertig MA, Li S, Li XJ (2017) MANF regulates hypothalamic control of food intake and body weight. Nat Commun 8:579. 
[3] Hong Y, Zhao T, Li XJ, Li S (2017) Mutant Huntingtin Inhibits αB-Crystallin Expression and Impairs Exosome Secretion from Astrocytes. J Neurosci 37:9550-9563. 
[4] Li XJ, Tu Z, Yang W, Li S (2017) CRISPR: Established Editor of Human Embryos? Cell Stem Cell 21:295-296. 
[5] Zhao T, Hong Y, Yin P, Li S, Li XJ (2017) Differential HspBP1 expression accounts for the greater vulnerability of neurons than astrocytes to misfolded proteins. Proc Natl Acad Sci U S A 114:E7803-E7811.


 Shinn-Zong (John) Lin, M.D., Ph.D.

 Professor, Department of Neurosurgery
 Tzu Chi Medical University
 Hualien, Taiwan, China

 

 

 

Special Expertise
Neuroscience
Neurosurgery
Stem Cell Therapies
Translational Science
New Drug Development
Hospital Management

Selected Recent Publications
[1] Ting HC, Chang CY, Lu KY, Chuang HM, Tsai SF, Huang MH, Liu CA, Lin SZ, Harn HJ (2018) Targeting Cellular Stress Mechanisms and Metabolic Homeostasis by Chinese Herbal Drugs for Neuroprotection. Molecules 23:E259.
[2] Fan HC, Chi CS, Chang YK, Tung MC, Lin SZ, Harn HJ (2018) The Molecular Mechanisms of Plant-Derived Compounds Targeting Brain Cancer. Int J Mol Sci 19:E395. 
[3] Rajamani K, Liu JW, Wu CH, Chiang IT, You DH, Lin SY, Hsieh DK, Lin SZ, Harn HJ, Chiou TW (2017) n-Butylidenephthalide exhibits protection against neurotoxicity through regulation of tryptophan 2, 3 dioxygenase in spinocerebellar ataxia type 3. Neuropharmacology 117:434-446. 
[4] Tsai CW, Tsai RT, Liu SP, Chen CS, Tsai MC, Chien SH, Hung HS, Lin SZ, Shyu WC, Fu RH (2017) Neuroprotective Effects of Betulin in Pharmacological and Transgenic Caenorhabditis elegans Models of Parkinson's Disease. Cell Transplant 26:1903-1918. 
[5] Hsieh J, Liu JW, Harn HJ, Hsueh KW, Rajamani K, Deng YC, Chia CM, Shyu WC, Lin SZ, Chiou TW (2017) Human Olfactory Ensheathing Cell Transplantation Improves Motor Function in a Mouse Model of Type 3 Spinocerebellar Ataxia. Cell Transplant 26:1611-1621.


 Dana M. McTigue, Ph.D.

 Professor, Department of Neuroscience
 Vice Chair, Center for Brain and Spinal Cord Repair
 The Ohio State University College of Medicine
 Columbus, OH, USA

 

 

Research Interests:
Spinal cord injury and recovery of function
Gliogenesis
Adult progenitor cell function
Demyelination and remyelination of the CNS

Current Research: Dr. McTigue's laboratory focuses on the role of adult progenitor cells after CNS injury or disease. These cells have been shown to form new oligodendrocytes in vivo after demyelination, and to form oligodendrocytes, astrocytes and neurons in vitro. In  recent studies, they determined that these cells spontaneously form a large number of new oligodendrocytes and remyelinate axons for several months after spinal cord injury. This work has relevance not only to traumatic injury but also conditions such as multiple sclerosis and even normal aging.
In ongoing studies, they are examining: 1) What molecules present after spinal cord injury promote this robust endogenous reparative response; 2) What effect inflammation has on the this spontaneous repair; 3) What type of intercellular communications are involved in gliogenesis after CNS injury, including interactions between progenitors, astrocytes, oligodendrocytes, microglia and macrophages.
The long-term goal of these studies is to determine how the formation of new cells in the adult CNS is regulated and whether this process can be manipulated to promote greater anatomical and functional recovery from spinal cord injury and other CNS disorders.

Selected Recent Publications
[1] Du Y, Wang W, Lutton AD, Kiyoshi CM, Ma B, Taylor AT, Olesik JW, McTigue DM, Askwith CC, Zhou M (2018) Dissipation of transmembrane potassium gradient is the main cause of cerebral ischemia-induced depolarization in astrocytes and neurons. Exp Neurol303:1-11. 
[2] Hesp ZC, Yoseph RY, Suzuki R, Wilson C, Nishiyama A, McTigue DM (2017) Proliferating NG2 cell-dependent angiogenesis and scar formation alter axon growth and functional recovery after spinal cord injury in mice. J Neurosci doi:10.1523/JNEUROSCI.3953-16.2017. 
[3] Siu JJ, Queen NJ, Huang W, Yin FQ, Liu X, Wang C, McTigue DM, Cao L (2017) Improved gene delivery to adult mouse spinal cord through the use of engineered hybrid adeno-associated viral serotypes. Gene Ther 24:361-369. 
[4] Church JS, Milich LM, Lerch JK, Popovich PG, McTigue DM (2017) E6020, a synthetic TLR4 agonist, accelerates myelin debris clearance, Schwann cell infiltration, and remyelination in the rat spinal cord. Glia 65:883-899. 
[5] Blissett AR, Ollander B, Penn B, McTigue DM, Agarwal G (2017) Magnetic mapping of iron in rodent spleen. Nanomedicine 13:977-986.


 Hideyuki Okano, M.D., Ph.D.

 Professor, Dean,
 Department of Physiology
 Keio University School of Medicine
 Tokyo, Japan

 

 

Research Interests:
Our lab was the first in the world to successfully generate transgenic marmosets with germline transmission. Our gene modification techniques can be used in a variety of non-human primates. Through our study of genetically modified marmosets (including disease models), we aim to understand the higher cognitive functions that are unique to primates. Ultimately, we hope to apply our work in treating human neurologic diseases.
Little is known about the axonal connectivity and functional distribution in the marmoset brain. Thus, we also aim to create a structural and functional marmoset brain atlas by combining 9.4T MRI, tracer injection and Ca2+ imaging techniques.

Selected Recent Publications
[1] Izpisua Belmonte JC, Callaway EM, Caddick SJ, Churchland P, Feng G, Homanics GE, Lee KF, Leopold DA, Miller CT, Mitchell JF, Mitalipov S, Moutri AR, Movshon JA, Okano H, Reynolds JH, Ringach D, Sejnowski TJ, Silva AC, Strick PL, Wu J, Zhang F (2015) Brains, genes, and primates. Neuron 86:617-631. 
[2] Kuwako K, Nishimoto Y, Kawase S, Okano HJ, Okano H (2014) Cadherin-7 regulates mossy fiber connectivity in the cerebellum. Cell Rep 9:311-323. 
[3] Bae BI, Tietjen I, Atabay KD, Evrony GD, Johnson MB, Asare E, Wang PP, Murayama AY, Im K, Lisgo SN, Overman L, Šestan N, Chang BS, Barkovich AJ, Grant PE, Topçu M, Politsky J, Okano H, Piao X, Walsh CA (2014) Evolutionarily dynamic alternative splicing of GPR56 regulates regional cerebral cortical patterning. Science 343:764-768. 
[4] Naka-Kaneda H, Nakamura S, Igarashi M, Aoi H, Kanki H, Tsuyama J, Tsutsumi S, Aburatani H, Shimazaki T, Okano H (2014) The miR-17/106-p38 axis is a key regulator of the neurogenic-to-gliogenic transition in developing neural stem/progenitor cells. Proc Natl Acad Sci U S A 111:1604-1609.
[5] Bundo M, Toyoshima M, Okada Y, Akamatsu W, Ueda J, Nemoto-Miyauchi T, Sunaga F, Toritsuka M, Ikawa D, Kakita A, Kato M, Kasai K, Kishimoto T, Nawa H, Okano H, Yoshikawa T, Kato T, Iwamoto K (2014) Increased l1 retrotransposition in the neuronal genome in schizophrenia. Neuron 81:306-313.


 Zhiping P. Pang, M.D., Ph.D.
 Principal Investigator/Assistant Professor
 Child Health Institute of New Jersey
 Department of Neuroscience and Cell Biology
 Rutgers Robert Wood Johnson Medical School
 New Brunswick, NJ 08901, USA

 

 

Research Interests:
Mechanisms of synaptic regulation: From stem cell to the brain
My laboratory studies the neural basis of the regulation of feeding, satiety, metabolism and obesity. Our studies may provide insights into the neural causes and consequences of childhood obesity. We also developed novel techniques for deriving neuronal cells from primary skin cells and pluripotent stem cells, providing novel opportunities to study the pathogenesis of neurological disorders, including pediatric developmental disorders and autism spectrum disorders.
1) how peptidergic hormones including leptin, ghrelin and insulin, and neuropeptides including neuropeptide Y and proopiomelanocortin regulate synaptic functions with defined synaptic connections within the hypothalamic region in control and obese states, and to evaluate the behavioral outcomes in animals;
2) to unravel the molecular mechanisms of peptidergic regulation of synaptic functions in the hypothalamus;
3) to elucidate the molecular mechanisms of neuropeptide release in hypothalamic neurons regulated by peptidergic hormones.
4) to establish a cellular-based model using derived human neurons from pluripotent stem cells or fibroblasts for study of hormonal regulation on synaptic functions in human brain.

Selected Recent Publications
[1] Forrest MP, Zhang H, Moy W, McGowan H, Leites C, Dionisio LE, Xu Z, Shi J, Sanders AR, Greenleaf WJ, Cowan CA, Pang ZP, Gejman PV, Penzes P, Duan J (2017) Open Chromatin Profiling in hiPSC-Derived Neurons Prioritizes Functional Noncoding Psychiatric Risk Variants and Highlights Neurodevelopmental Loci. Cell Stem Cell 21:305-318.e8. 
[2] Lim CS, Kang X, Mirabella V, Zhang H, Bu Q, Araki Y, Hoang ET, Wang S, Shen Y, Choi S, Kaang BK, Chang Q, Pang ZP, Huganir RL, Zhu JJ (2017) BRaf signaling principles unveiled by large-scale human mutation analysis with a rapid lentivirus-based gene replacement method. Genes Dev 31:537-552. 
[3] Liu J, Pang ZP (2016) Glucagon-like peptide-1 drives energy metabolism on the synaptic highway. FEBS J 283:4413-4423. 
[4] Xue Y, Qian H, Hu J, Zhou B, Zhou Y, Hu X, Karakhanyan A, Pang Z, Fu XD (2016) Sequential regulatory loops as key gatekeepers for neuronal reprogramming in human cells. Nat Neurosci 19:807-815. 
[5] Carlson AL, Bennett NK, Francis NL, Halikere A, Clarke S, Moore JC, Hart RP, Paradiso K, Wernig M, Kohn J, Pang ZP, Moghe PV (2016) Generation and transplantation of reprogrammed human neurons in the brain using 3D microtopographic scaffolds. Nat Commun 7:10862.


 Bo Peng, Ph.D.

 Associate Professor, Principal Investigator (PI)
 Institute of Biomedical and Health Engineering (IBHE)
 Shenzhen Institutes of Advanced Technology (SIAT)
 Chinese Academy of Sciences (CAS), China

 

 

Overview
Dr. Bo Peng obtained his PhD degree from The University of Hong Kong. He mainly focused on retinal neurodegenerative disorders. By using diverse approaches, he studied the roles of microglia in retinitis pigmentosa, which is a photoreceptor-degenerative disorder in the retina. So far, he has published peer-reviewed papers in Journal of Neuroscience, Scientific Reports, and CNS Neuroscience & Therapeutics as the first or corresponding author. Besides, he is the reviewer of4 journals. In 2015, he has joined Shenzhen Institutes of Advanced Technology at Chinese Academy of Sciences as a PI and associate professor.


 Philip G. Popovich, Ph.D.

 Professor, Department of Neuroscience
 Director, Center for Brain and Spinal Cord Repair
 The Ohio State University College of Medicine
 Columbus, OH, USA

 

 

General Research: The Center for Brain and Spinal Cord Repair lab is an interdisciplinary research group dedicated to studying the complexities of CNS injury, inflammation and tissue repair. They are currently funded by the NIH to explore the consequences of resident (e.g., microglia) and recruited inflammatory cell (e.g., macrophages, T-lymphocytes) activation on axonal injury, demyelination and neurological function in models of rat and mouse SCI. Inflammation is an inevitable consequence of tissue damage and is necessary for efficient cell repair. However, acute inflammation also causes “collateral” damage to tissues before repair processes are initiated. In the spinal cord, where most cells are post-mitotic and exhibit poor regenerative/repair potential, inflammation can have devastating consequences. Theyare striving to develop novel therapies that will manipulate or over-ride normal immune function.

Research Interests:
Neuroimmunology of spinal cord injury
Immunological influences on neuronal degeneration and regeneration
Neuroendocrine influences (e.g., stress/HPA axis activation) on inflammatory mediated injury/repair of the CNS

Selected Recent Publications
[1] Kigerl KA, Mostacada K, Popovich PG (2018) Gut Microbiota Are Disease-Modifying Factors After Traumatic Spinal Cord Injury. Neurotherapeutics 15:60-67. 
[2] Goldstein EZ, Church JS, Pukos N, Gottipati MK, Popovich PG, McTigue DM (2017) Intraspinal TLR4 activation promotes iron storage but does not protect neurons or oligodendrocytes from progressive iron-mediated damage. Exp Neurol 298:42-56.
[3] Freria CM, Hall JC, Wei P, Guan Z, McTigue DM, Popovich PG (2017) Deletion of the Fractalkine Receptor, CX3CR1, Improves Endogenous Repair, Axon Sprouting, and Synaptogenesis after Spinal Cord Injury in Mice. J Neurosci 37:3568-3587. 
[4] Church JS, Milich LM, Lerch JK, Popovich PG, McTigue DM (2017) E6020, a synthetic TLR4 agonist, accelerates myelin debris clearance, Schwann cell infiltration, and remyelination in the rat spinal cord. Glia 65:883-899. 
[5] Kigerl KA, Hall JC, Wang L, Mo X, Yu Z, Popovich PG (2016) Gut dysbiosis impairs recovery after spinal cord injury. J Exp Med 213:2603-2620.


 Limin Rong, M.D., Ph.D.

 Professor, President of the 3rd Affiliated Hospital of Sun Yat-Sen University (SYSU)
 Director and Academic Leader of Orthopaedic & Spine Department of the 3rd Affiliated Hospital of SYSU
 Director of Minimally Invasive Spine Surgery Center of SYSU
 Co-director of Clinical Center of Spinal Cord Injury Research Institution of SYSU, China

 

 

Research Interests
Minimally Invasive Spine Surgery (MISS)
Controls of Stem Cell Differentiation and Musculoskeletal Development
Mechanism, Prevention and Treatment of Osteoporosis
Musculoskeletal Tissue Regeneration and Tissue Engineering
Stem Cell Clinical Applications and Translational Research: Spinal Cord Injury
Immune Function of the Skeletal System

Selected Recent Publications
[1] Zhang L, Chen R, Liu B, Zhang W, Zhu Y, Rong L (2017) The nerve root sedimentation sign for differential diagnosis of lumbar spinal stenosis: a retrospective, consecutive cohort study. Eur Spine J 26:2512-2519.
[2] Shu T, Pang M, Rong L, Liu C, Wang J, Zhou W, Wang X, Liu B (2015) Protective Effects and Mechanisms of Salvianolic Acid B Against H?O?-Induced Injury in Induced Pluripotent Stem Cell-Derived Neural Stem Cells. Neurochem Res 40:1133-1143. 
[3] Liu C, Huang Y, Pang M, Yang Y, Li S, Liu L, Shu T, Zhou W, Wang X, Rong L, Liu B (2015) Tissue-engineered regeneration of completely transected spinal cord using induced neural stem cells and gelatin-electrospun poly (lactide-co-glycolide)/polyethylene glycol scaffolds. PLoS One 10:e0117709. 
[4] Zhang L, Chen R, Xie P, Zhang W, Yang Y, Rong L (2015) Diagnostic value of the nerve root sedimentation sign, a radiological sign using magnetic resonance imaging, for detecting lumbar spinal stenosis: a meta-analysis. Skeletal Radiol 44:519-527.
[5] Zhou W, Xie P, Pang M, Yang B, Fang Y, Shu T, Liu C, Wang X, Zhang L, Li S, Rong L (2015) Upregulation of CRMP4, a new prostate cancer metastasis suppressor gene, inhibits tumor growth in a nude mouse intratibial injection model. Int J Oncol 46:290-298.


 John T. Povlishock, Ph.D.

 Professor and Chair, Department of Anatomy and Neurobiology
 Director, Commonwealth Center for the Study of Brain Injury
 Virginia Commonwealth University School of Medicine
 Richmond, Virginia, USA
 Editor-in-Chief of the Journal of Neurotrauma

 

 

Overview
Dr. John Povlishock is Chair of Anatomy and Neurobiology on the Medical College of Virginia Campus of Virginia Commonwealth University.  He serves as Editor-in-Chief of the Journal of Neurotrauma, as well as the Director of the Commonwealth Center for the Study of Brain Injury.  His research focuses on traumatic brain injury, with emphasis on neuroprotection, targeting neuronal, axonal, and vascular change. His work has been reported in over 200 papers, reviews, books, and chapters which, to date, have been cited over 17,000 times. For his research accomplishments, he has received two Javits Neuroscience Investigator Awards from the National Institute of Neurological Disorders and Stroke, which also awarded him their Gold Medal for Brain Injury Research.  He has also received the Caveness Award from the National Head Injury Foundation, the Brain Trauma Lecture Award from the Joint Congress of Neurological Surgery, the Bass Lecturer Award from the Society of Neurological Surgeons, the Peter and Eva Safar Lecture Award from the University of Pittsburgh, and the Deborah L. Warden Lectureship from the Defense and Veterans Brain Injury Center.  In 2006, Dr. Povlishock was the recipient of the Commonwealth of Virginia’s Outstanding Scientist Award while in 2011, he was awarded a Doctor of Science Degree (honoris causa) from the University of Pécs in Hungary. Over his 42 year academic career he has served as a chartered member and chair of numerous NIH review panels, while also serving as chair of the VA merit review system in neuroscience and the Commonwealth of Kentucky’s Brain and Spinal Cord Injury Research Trust review panel. He recently completed four years of service on the National Advisory Neurological Disorders and Stroke Council of the National Institutes of Health.


 Christopher B. Shields, M.D.

 Professor
 Norton Neuroscience Institute
 Norton Healthcare
 Louisville, KY, USA

 

 

Overview
Christopher Shields, M.D., earned his medical degree from the University of Toronto in Ontario, Canada. He completed his internship at St. Michael's Hospital at the University of Toronto and his residency at the University of Manitoba in Winnipeg. Dr. Shields completed a fellowship in microvascular neurosurgery at the University of Vermont in Burlington. He is board certified by the Royal College of Physicians and Surgeons of Canada, the American Board of Neurological Surgery, as well as several other professional medical associations
Our specialty practice is a part of Norton Medical Group, a multispecialty physician group at Norton Healthcare. Norton Medical Group currently includes providers who offer primary, specialty and urgent care services in locations throughout Kentucky and Southern Indiana. Our practice is comprised of compassionate, skilled specialists who are committed to ensuring you receive the best care and have access to the latest medical technology and services.


 Kwok-fai So, Ph.D.

 Member, Chinese Academy of Sciences
 The University of Hong Kong
 GHM Institute of CNS Regeneration,
 Jinan University
 Guangzhou, China

 

 

Overview
Director of GHM Institute of CNS Regeneration at Jinan University, Guangzhou, China; Chair of Anatomy in the Department of Ophthalmology and the State Key Laboratory of Brain and Cognitive Sciences, Jessie Ho Professor in Neuroscience, The University of Hong Kong; (http://www.eyeinst.hku.hk/Prof_So.htm), member of the Chinese Academy of Sciences, member of the Advisory Committee/ 2011 Program, member of Consultative Committee/ the national 973 Program (www.973.gov.cn/), Director of China Spinal Cord Injury Network (ChinaSCINet), Director of Hong Kong Spinal Cord Injury Fund (HKSCIF), Co-Chairman of the Board of Director of the ChinaSCINet (www.chinascinet.org ), and  Editor-in-Chief of Neural Regeneration Research (www.nrronline.org ). Received Ph.D. degree from MIT. He is one of the pioneers in the field of axonal regeneration in visual system. He was the first to show lengthy regeneration of retinal ganglion cells in adult mammals with peripheral nerve graft. He is currently using multiple approaches to promote axonal regeneration in the optic nerve and spinal cord. His team identifies neuroprotective and regenerative factors including: exercise, wolfberry, trophic factors, peptide nanofiber scaffold, and environmental manipulation. 1995 obtained the Natural Science Award of the National Natural Science Foundation of China. 1999 was elected Member of the Chinese Academy of Sciences. 2015 was elected US National Academy of Invention Fellow. He is the author and co-author of over 380+ publications ( http://scholar.google.com/citations?hl=en&user=SUPKYiQAAAAJ&view_op=list_works ); co-inventors of 23 patents.

Selected Recent Publications
[1] Shi L, Guo Y, Dong C, Huddleston J, Yang H, Han X, Fu A, Li Q, Li N, Gong S, Lintner KE, Ding Q, Wang Z, Hu J, Wang D, Wang F, Wang L, Lyon GJ, Guan Y, Shen Y, Evgrafov OV, Knowles JA, Thibaud- Nissen F, Schneider V, Yu CY, Zhou L, Eichler EE, So KF, Wang K (2016) Long-read sequencing and de novo assembly of a Chinese genome. Nat Commun 7:12065.
[2] Zhang T, Huang L, Zhang L, Tan M, Pu M, Pickard GE, So KF, Ren C (2016) ON and OFF retinal ganglion cells differentially regulate serotonergic and GABAergic activity in the dorsal raphe nucleus. Sci Rep 6:26060. 
[3] Leung JW, Lau BW, Chan VS, Lau CS, So KF (2016) Abnormal increase of neuronal precursor cells and exacerbated neuroinflammation in the corpus callosum in murine model of systemic lupus erythematosus. Restor Neurol Neurosci 34:443-453. 
[4] Li HY, Ruan YW, Kau PW, Chiu K, Chang RC, Chan HH, So KF (2015) Effect of Lycium barbarum (Wolfberry) on alleviating axonal degeneration after partial optic nerve transection. Cell Transplant 24):403-417.
[5] Yau SY, Li A, Hoo RL, Ching YP, Christie BR, Lee TM, Xu A, So KF (2014) Physical exercise-induced hippocampal neurogenesis and antidepressant effects are mediated by the adipocyte hormone adiponectin. Proc Natl Acad Sci U S A 111:15810-15815.


 Tao Sun, Ph.D.

 Professor
 President of Ningxia Medical University
 Director of key cerebrocranial disease labtorary in Ningxia
 Chief surgeon in neurosurgery, Ningxia Medical University

 

 

Overview
As the leading person in neurosurgery in Ningxia, Prof. Sun Tao has high attainments in central nervous system tumor surgery and functional neurosurgery, especially in the surgical treatment of eplipsy. He has attached special attention to Insular Epilepsy, as he has done a series of basic ad clinical researches in term of insular anatomy and epilepsy pathogenesis and with  the treatise “On Insular Epilepsy” published.  Currently, he is in charge of initial-stage special research of “973” project - national key basic research development plan,  and many other research programs, including that of National Natural Science Funds, the Sci-tech research program of the Autonomous Region and Natural Science Funds, etc. In recent years he has published more than 120 academic theses at home and abroad. In addition, he is the chief editor of 3 treaties on neurosurgery and participated in 7 treaties, and chief editor in the complication of 5 teaching materials for universities. Owing to his outstanding performance and achievements, he has been awarded over 20 various provincial level prizes (including 3 first prize and 7 second prize in Sci-tech progress of the Region).

Selected Recent Publications:
[1] Yang X, Hei C, Liu P, Song Y, Thomas T, Tshimanga S, Wang F, Niu J, Sun T, Li PA (2015) Inhibition of mTOR pathway by Rapamycin reduces brain damage in rats subjected to transient forebrain ischemia. Int J Biol Sci 11:1424-1435.
[2] Zhao P, Zhou R, Li HN, Yao WX, Qiao HQ, Wang SJ, Niu Y, Sun T, Li YX, Yu JQ (2015) Oxymatrine attenuated hypoxic-ischemic brain damage in neonatal rats via improving antioxidant enzyme activities and inhibiting cell death. Neurochem Int 89:17-27.
[3] Wang T, Li Y, Wang Y, Zhou R, Ma L, Hao Y, Jin S, Du J, Zhao C, Sun T, Yu J (2014) Lycium barbarum polysaccharide prevents focal cerebral ischemic injury by inhibiting neuronal apoptosis in mice. PLoS One 9:e90780.
[4] Wang YS, Li YX, Zhao P, Wang HB, Zhou R, Hao YJ, Wang J, Wang SJ, Du J, Ma L, Sun T, Yu JQ (2015) Anti-inflammation efects of oxysophoridine on ceredral on cerebral ischemia-reperfusion injury in mice. Inflammation 38:2259-2268.
[5] Zhao P, Zhou R, Zhu XY, Hao YJ, Li N, Wang J, Niu Y, Sun T, Li YX, Yu JQ (2015) Matrine attenuated focal cerebral ischemic injury via improving anti-oxidant activity and inhibiting apoptosis in mice. Int J Mol Med 36:633-644.


 Yi Sun, Ph.D.

 Professor, Tongji University School of Medicine, China
 Associate Professor, Psychiatry and Biobehavioral Sciences
 Associate Professor In-Residence, Semel Institute for Neuroscience and Human Behavior
 Brain Research Institute
 University of California, Los Angeles, CA, USA

 

 

Research Interests
Neural stem cells (NSC) are immature cells capable of generating all three major cell types in the central nervous system (CNS), neurons, astrocytes, and oligodendrocytes. That they are multipotent and have the ability to self-renew makes NSC good candidates for repairing damage in the CNS and treating neurodegenerative diseases. The research in our laboratory is aimed at understanding the molecular mechanisms by which cell-fate decisions, cell proliferation and differentiation are controlled in NSC. Both extracellular /environmental factors and cell intrinsic programs influence stem cell proliferation and differentiation. For example, our previous studies have shown that the cytokines leukemia inhibitory factor (LIF) and cilliary neurotrophic factor (CNTF), through activation of the JAK (Janus Kinase)/STAT (signal transducers and activators of transcription) signaling pathway, effectively turn on astrocyte specific genes leading NSC to differentiate into astrocytes (Science 1997, 278: 477-483). Recently, we found that a cell intrinsic factor, the basic helix-loop-helix transcription factor neurogenin1, When expressed in these cells, triggers a cascade of neuronal gene activation and at the same time suppresses glial genes, resulting in neurogenesis (Cell 2001, 104: 365-376). Changes in gene expression patterns are key events during cell cycle exit and cell differentiation. Therefore our future research will focus on elucidating, 1. the role of transcription factors such as STATs and neurogenic transcription factors in turning on and off specific gene expression programs related to proliferation and differentiation, and 2. how extracellular factors including LIF, FGF-2, PDGF and BMPs and intracellular signaling pathways (e.g. Ras-MAPkinase, PI3Kinase-AKT and JAK-STAT pathways) regulate the activities of these transcription factors. Currently we are developing a method which will allow us to efficiently derive pure NSC cultures from mouse embryonic stem cells (ES cells). Since these cells are easily genetically modifiable, we will be able to manipulate gene expression through state of the art transgenic or knockout technology in ES cells, then convert the transgenic ES cells into NSC and study the impact of these genes in the proliferation and differentiation of NSC. Understanding the molecular control of cell fate choice will allow us to direct the differentiation of NSC and to genetically engineer NSC (via ES cells) so that they may be suitable in cell replacement therapies for neurological disorders such as Alzheimer's and Parkinson's diseases.

Selected Recent Publications:
[1] Sheng Z, Sun Y, Yin Z, Tang K, Cao Z (2017) Advances in computational approaches in identifying synergistic drug combinations. Brief Bioinform doi:10.1093/bib/bbx047.
[2] Sun Y, Sheng Z, Ma C, Tang K, Zhu R, Wu Z, Shen R, Feng J, Wu D, Huang D, Huang D, Fei J, Liu Q, Cao Z (2015) Combining genomic and network characteristics for extended capability in predicting synergistic drugs for cancer. Nat Commun 6:8481.
[3] Sheng Z, Sun Y, Zhu R, Jiao N, Tang K, Cao Z, Ma C (2015) Functional Cross-Talking between Differentially Expressed and Alternatively Spliced Genes in Human Liver Cancer Cells Treated with Berberine. PLoS One 10:e0143742. 
[4] Fu P, Yang L, Sun Y, Ye L, Cao Z, Tang K (2014) Target network differences between western drugs and Chinese herbal ingredients in treating cardiovascular disease. BMC Bioinformatics 4:S3. 
[5] Kang H, Tang K, Liu Q, Sun Y, Huang Q, Zhu R, Gao J, Zhang D, Huang C, Cao Z (2013) HIM-herbal ingredients in-vivo metabolism database. J Cheminform 5:28.


 Andrea Tedeschi, Ph.D.

 Associate Professor
 Department of Neuroscience, College of Medicine
 The Ohio State University - Wexner Medical Center,
 USA

 

 

Research Interests:
Traumatic brain and spinal cord injuries cause profound neurological deficits and long-term disability due to detrimental alterations in structure and function of neuronal circuits. Although axonal injury is associated with several neurobehavioral and neuropathological characteristics, how changes in intrinsic neuronal properties alter interaction between neurons and non-neuronal cells remains a central mystery in neuroscience.  Much of the progress to address this question has come from either studies that use in vitro surrogate models or in vivo endpoint studies.  These experimental models, however, do not provide the spectrum of variables that influence the behavioral or systemic changes that occur in response to CNS trauma.  It is our goal to shed some light on this important research topic and decipher the coding principle altering neuron circuit structure and function.
To achieve this goal, we take advantage of a multidisciplinary approach that combines transcriptomics, bioinformatics, genetic, molecular and pharmacological approaches together with in vivo time-lapse multiphoton microscopy and whole-body optical clearing.  By taking this innovative approach, we will begin to understand how to manipulate the self-repair mechanisms of the brain and spinal cord and help to design specific therapies aimed to improve neurological function and quality of life in individuals afflicted by traumatic CNS injury.

Selected Recent Publications
[1] Prüss H, Tedeschi A, Thiriot A, Lynch L, Loughhead SM, Stutte S, Mazo IB, Kopp MA, Brommer B, Blex C, Geurtz LC, Liebscher T, Niedeggen A, Dirnagl U, Bradke F, Volz MS, DeVivo MJ, Chen Y, von Andrian UH, Schwab JM (2017) Spinal cord injury-induced immunodeficiency is mediated by a sympathetic-neuroendocrine adrenal reflex. Nat Neurosci 20:1549-1559.
[2] Tedeschi A, Bradke F (2016) Spatial and temporal arrangement of neuronal intrinsic and extrinsic mechanisms controlling axon regeneration. Curr Opin Neurobiol 42:118-127.
[3] Tedeschi A, Dupraz S, Laskowski CJ, Xue J, Ulas T, Beyer M, Schultze JL, and Bradke F (2016) The calcium channel subunit Alpha2delta2 suppresses axon regeneration in the adult CNS. Neuron 92:419-434. 
[4] Omura T, Omura K, Tedeschi A, Riva P, Painter M, Rojas L, Martin J, Lisi V, Huebner E, Latremoliere A, Yin Y, Barrett L, Singh B, Lee S, Crisman T, Gao F, Li S, Kapur K, Geschwind DH, Kosik KS, Coppola G, He Z, Carmichael ST, Benowitz LI, Costigan M, Woolf CJ (2015) Robust axonal regeneration occurs in the injured CAST/Ei mouse CNS. Neuron 86:1215-1227.
[5] Ruschel J, Hellal F*, Flynn KC*, Dupraz S*, Elliot DA, Tedeschi A, Bates M, Sliwinski C, Brook G, Dobrint K, Peitz M, Brüstle O, Norenberg MD, Blesch A, Weidner N, Bunge MB, Bixby JL, Bradke F (2015) Systemic administration of epothilone B promotes axon regeneration after spinal cord injury. Science 348:347-352.


 Veronica Tom, Ph.D.

 Associate Professor
 Department of Neurobiology and Anatomy
 Drexel University College of Medicine
 Philadelphia, PA, USA

 

 

Research Interests:
Injury to the spinal cord interrupts input to and from the brain. Because adult central nervous system axons fail to fully regenerate following injury, severed axons are permanently disconnected from their target neurons. This results in deficits in voluntary motor function (e.g., walking), involuntary motor function (e.g., diaphragmatic activity for respiration), autonomic function (e.g., cardiovascular regulation, bladder function) and sensation.
The research mission of the lab is to develop strategies to promote recovery of these affected behaviors after acute and chronic spinal cord injury.
We are focused on two general research projects:
--Enhancing axon regeneration
--Mitigating autonomic dysfunction after spinal cord injury
Our highly collaborative research involves a multitude of techniques, including survival surgery, cell transplantation, gene manipulation, cell culture, assessment of cardiovascular function, and tests to gauge locomotor and sensory function.

Selected Recent Publications
[1] Wang Z, Nong J, Shultz RB, Zhang Z, Kim T, Tom VJ, Ponnappan RK, Zhong Y (2017) Local delivery of minocycline from metal ion-assisted self-assembled complexes promotes neuroprotection and functional recovery after spinal cord injury. Biomaterials 112:62-71. 
[2] Hou S, Carson DM, Wu D, Klaw MC, Houlé JD, Tom VJ (2016) Dopamine is produced in the rat spinal cord and regulates micturition reflex after spinal cord injury. Exp Neurol 285:136-146. 
[3 Wu D, Klaw MC, Kholodilov N, Burke RE, Detloff MR, Côté MP, Tom VJ (2016) Expressing Constitutively Active Rheb in Adult Dorsal Root Ganglion Neurons Enhances the Integration of Sensory Axons that Regenerate Across a Chondroitinase-Treated Dorsal Root Entry Zone Following Dorsal Root Crush. Front Mol Neurosci 9:49.
[4] Goldberg JL, Guido W; Agi Workshop Participants (2016) Report on the National Eye Institute Audacious Goals Initiative: Regenerating the Optic Nerve. Invest Ophthalmol Vis Sci 57:1271-1275. 
[5] Partida E, Mironets E, Hou S, Tom VJ (2016) Cardiovascular dysfunction following spinal cord injury. Neural Regen Res 11:189-194.


 Scott R. Whittemore, Ph.D.

 Professor and Vice Chairman for Research
 Department of Neurological Surgery, Anatomical Sciences & Neurobiology
 Kentucky Spinal Cord Injury Research Center
 University of Louisville, School of Medicine
 Louisville, KY, USA

 

 

Research Focus:
Spinal Cord Injury causes many changes at the molecular level that damage or destroy key components of the nervous system that carry signals to and from the brain - including neurons, axons and the myelin coating that protects the nervous system much like the insulation around an electrical cord, as well as the vascular infrastructure that carries oxygen to these tissues.
Find strategies to replace lost neurons, help axons regenerate, and regeneration of the myelin coating around damaged or regenerating axons.
Using undifferentiated precursor cells, gene therapies, and transplanted neurons, the lab seeks to understand the development of these key components of the vascular and nervous system at the molecular and genetic level in order to protect them from damage and/or promote their regeneration.

Selected Recent Publications
[1] Pocratsky AM, Burke DA, Morehouse JR, Beare JE, Riegler AS, Tsoulfas P, States GJR, Whittemore SR, Magnuson DSK (2017) Reversible silencing of lumbar spinal interneurons unmasks a task-specific network for securing hindlimb alternation. Nat Commun 8:1963. 
[2] Kuypers NJ, Bankston AN, Howard RM, Beare JE, Whittemore SR (2016) Remyelinating Oligodendrocyte Precursor Cell miRNAs from the Sfmbt2 Cluster Promote Cell Cycle Arrest and Differentiation. J Neurosci 36:1698-1710.
[3] Nielson JL, Guandique CF, Liu AW, Burke DA, Lash AT, Moseanko R, Hawbecker S, Strand SC, Zdunowski S, Irvine KA, Brock JH, Nout-Lomas YS, Gensel JC, Anderson KD, Segal MR, Rosenzweig ES, Magnuson DS, Whittemore SR, McTigue DM, Popovich PG, et al. (2014) Development of a database for translational spinal cord injury research. J Neurotrauma 31:1789-1799. 
[4] Myers SA, Andres KR, Hagg T, Whittemore SR (2014) CD36 deletion improves recovery from spinal cord injury. Exp Neurol 256:25-38.
[5] Ohri SS, Hetman M, Whittemore SR (2013) Restoring endoplasmic reticulum homeostasis improves functional recovery after spinal cord injury. Neurobiol Dis 58:29-37.


 Junfang Wu, B.M., Ph.D.

 Associate Professor
 Department of Anesthesiology and Center for Shock, Trauma and Anesthesiology Research
 School of Medicine, University of Maryland, USA

 

 

 

Biosketch
The overall objective of research in my laboratory is to examine secondary injury processes following traumatic spinal cord injury (SCI) and pharmacological/gene therapeutic interventions for SCI. Specifically, we focus on: (1) Elucidating molecular mechanisms responsible for SCI-induced brain inflammation. This may lead to effective therapeutic interventions that limit post-SCI cognitive decline and depression; (2) Demonstrating the function and the mechanisms of autophagy-lysosomal pathway and specific microRNAs in neuronal injury after SCI which could open a potential novel treatment avenue against SCI as well as identify candidate molecular targets for these manipulations; (3) Identifying the genetic and genomic factors that impact SCI-PAIN as well as identifying new therapeutic targets to reduce or eliminate SCI-PAIN, including a truncated isoform of the BDNF receptor tropomyosin related kinase B (trkB), trkB.T1; (4) Examining the function and mechanism of NOX2 on nocifensive behaviors and central pain regulation after experimental SCI and traumatic brain injury (TBI). My ultimate goal is to understand the cellular and molecular mechanism of functional recovery after SCI and also to develop potentially therapeutic strategies.

Research/Clinical Keywords
Spinal cord injury, brain injury, inflammation, autophagy-lysosomal, neuropathic pain, NOX2, cell cycle pathway, microRNA, motor function, cognition, depression, neurons, astrocytes, microglia

Selected Recent Publications
[1] Matyas JJ, O’Driscoll CM, Yu L, Coll-Miro M, Daugherty S, Renn CL, Faden AI, Dorsey SG, Wu J (2017) Truncated TrkB.T1-mediated astrocytes dysfunction contributes to impaired motor function and neuropathic pain after spinal cord injury. J Neuroscience 37: 3956-3971.
[2] Liu S, Sarkar C, Dinizo M, Faden AI, Koh EY, Lipinski MM, Wu J (2015). Disrupted autophagy after spinal cord injury is associated with ER stress and neuronal cell death. Cell Death Dis 6:e1582.
[3] Wu J, Zhao Z, Sabirzhanov B, Stoica BA, Kumar A, Luo T, Skovira J, Fade AI (2014). Spinal cord injury causes brain inflammation associated with cognitive and affective changes: role of cell cycle pathways. Jf Neuroscience 34:10989-11006. 
[4] Wu J, Renn CL, Faden AI, Dorsey SG (2013) TrkB.T1 contributes to neuropathic pain following spinal cord Injury through regulation of cell cycle pathways. J Neuroscience 33:12447-12463.
[5] Wu J, Yoo S, Wilcock D, Lytle LM, Leung PY, Colton CA, Wrathall JR (2010) Interaction of NG2+ glial progenitors and microglia/macrophages from the injured spinal cord. Glia 58:410-422.


 Xiao-Ming Xu, M.D., Ph.D.

 Scientific Director
 Spinal Cord and Brain Injury Research Group
 Stark Neurosciences Research Institute
 Indiana University School of Medicine, USA

 

 

Research Overview
Dr. Xu’s research has focused on the development, plasticity, and regeneration of the injured spinal cord. A major breakthrough from his research showed that Schwann cells, a type of peripheral nerve-derived glial cell, can promote axons of the central nervous system to regenerate across a spinal cord lesion gap and, when combined with appropriate trophic factors, can promote axonal reentry into the host spinal cord. A second line of Dr. Xu’s research has been neuroprotection against spinal cord injury-induced secondary cell death and tissue damage. He and his team are particularly interested in targeting an enzyme named phospholipase A2 as a central molecule that mediates multiple injury insults after the spinal cord injury, and screening therapeutic agents that can block phospholipase A2-mediated injury cascades. Dr. Xu hopes that eventually these neuroprotection and regeneration strategies can be combined to achieve maximal therapeutic effects. He also hopes that results from his research will be transferred to clinical treatments of patients with spinal cord injuries.

Selected Recent Publications
[1] Deng L, Ruan Y, Chen C, Frye CC, Xiong W, Jin X, Jones K, Sengelaub D, Xu XM (2015) Characterization of dendritic morphology and neurotransmitter phenotype of thoracic descending propriospinal neurons after complete spinal cord transection and GDNF treatment. Exp Neurol 277:103-114. 
[2] Wang H, Liu NK, Zhang YP, Deng L, Lu QB, Shields CB, Walker MJ, Li J, Xu XM (2015) Treadmill training induced lumbar motoneuron dendritic plasticity and behavior recovery in adult rats after a thoracic contusive spinal cord injury. Exp Neurol 271:368-378. 
[3] Walker CL, Wang X, Bullis C, Liu NK, Lu Q, Fry C, Deng L, Xu XM (2015) Biphasic bisperoxovanadium administration and Schwann cell transplantation for repair after cervical contusive spinal cord injury. Exp Neurol 264:163-172.
[4] Liu NK, Deng LX, Zhang YP, Lu QB, Wang XF, Hu JG, Oakes E, Bonventre JV, Shields CB, Xu XM (2014) Cytosolic phospholipase A2 protein as a novel therapeutic target for spinal cord injury. Ann Neurol 75:644-658. 
[5] Wu W, Lee SY2, Wu X, Tyler JY, Wang H, Ouyang Z, Park K, Xu XM, Cheng JX (2013) Neuroprotective ferulic acid (FA)-glycol chitosan (GC) nanoparticles for functional restoration of traumatically injured spinal cord. Biomaterials 35:2355-2364.


 Zhengqin Yin, Ph.D.

 Professor and Director of Southwest Eye Hospital
 Third Military Medical University,Chongqing, China

 

 

 

 Overview

Dr. Zheng Qin Yin is currently the Professor and Director of Southwest Eye Hospital, Third Military Medical University, Chongqing, China. She is the Vice-President of Chinese Ophthalmology Society. Chair of Chinese Visual Physiology and Visual Science committee in Chinese Ophthalmology Society. Dr. Zheng Qin Yin concentrated on research majored in: 1. Basic and clinical research in retinal degeneration diseases, 2. Mechanism of plasticity in vision development, and clinical basic research of pediatric eye diseases. Her lab got international recognized achievement in neuro-blindness eye diseases, especially in retinal degeneration diseases, in which she led cell therapy study including retinal progenitor cells, bone-marrow stem cells, Olfactory ensheathing cells and etc. The clinical trial of retinal progenitor cells for RP and hESC-RPE for wetAMD stand at the leading edge in China.


 Wise Young, M.D., Ph.D.

 Distinguished Professor, Founding Director
 W. M. Keck Center for Collaborative Neuroscience
 Richard H. Shindell Chair in Neuroscience
 Rutgers University School of Arts and Sciences
 Piscataway, NJ, USA

 

 

Overview and Research Interests:
Dr. Wise Young, founding director of the W. M. Keck Center for Collaborative Neuroscience and a distinguished professor, is recognized as one of the world's outstanding neuroscientists. 
Dr. Young is committed to bringing treatments to people with spinal cord Injuries. He built and trained a twenty-five center clinical trial network in China, Taiwan, and Hong Kong where human clinical trials using umbilical cord blood mononuclear cells and lithium are underway. In the initial results from the Phase II trial in Kunming, China, 75% of the participants (15 out of 20) recovered walking with a rolling walker. He is establishing clinical trial networks in the United States, Norway, and India and will start Phase IIB Trials in 2016 and Phase III trials in 2017.
Dr. Young led the team that discovered and established high-dose methylprednisolone (MP) as the first effective therapy for spinal cord injuries. This 1990 work upended concepts that spinal cord injuries were permanent, refocused research, and opened new vistas of hope. He also developed the first standardized rat spinal cord injury model used worldwide for testing therapies, formed the first consortium funded by the National Institutes of Health (NIH) to test promising therapies, and helped establish several widely accepted clinical outcome measures in spinal cord injury research. Dr. Young founded and served as editor-in-chief of the Journal of Neurotrauma. He organized the International and National Neurotrauma Societies as forums for scientists to collaborate on spinal cord injury and brain research. He served on advisory committees for the NIH, National Academy of Sciences, and NICHD, and on many spinal cord injury advisory boards.

Selected Recent Publications
[1] Oettl LL, Ravi N, Schneider M, Scheller MF, Schneider P, Mitre M, da Silva Gouveia M, Froemke RC, Chao MV, Young WS, Meyer-Lindenberg A, Grinevich V, Shusterman R, Kelsch W (2016) Oxytocin Enhances Social Recognition by Modulating Cortical Control of Early Olfactory Processing. Neuron 90:609-621. 
[2] Zhu H, Poon W, Liu Y, Leung GK, Wong Y, Feng Y, Ng SCP, Tsang KS, Sun DTF, Yeung DK, Shen C, Niu F, Xu Z, Tan P, Tang S, Gao H, Cha Y, So KF, Fleischaker R, Sun D, et al. (2016) Phase I-II Clinical Trial Assessing Safety and Efficacy of Umbilical Cord Blood Mononuclear Cell Transplant Therapy of Chronic Complete Spinal Cord Injury. Cell Transplant 25:1925-1943.
[3] Guo L, Rolfe AJ, Wang X, Tai W, Cheng Z, Cao K, Chen X, Xu Y, Sun D, Li J, He X, Young W, Fan J, Ren Y (2016) Rescuing macrophage normal function in spinal cord injury with embryonic stem cell conditioned media. Mol Brain 9:48. 
[4] Gu N, Peng J, Murugan M, Wang X, Eyo UB, Sun D, Ren Y, DiCicco-Bloom E, Young W, Dong H, Wu LJ (2016) Spinal Microgliosis Due to Resident Microglial Proliferation Is Required for Pain Hypersensitivity after Peripheral Nerve Injury. Cell Rep 16:605-614. 
[5] Carmel JB, Young W, Hart RP (2015) Flipping the transcriptional switch from myelin inhibition to axon growth in the CNS. Front Mol Neurosci 8:34.


 Xinguang Yu, Ph.D.

 Professor, Chief, Department of Neurosurgery
 Chinese PLA General Hospital, Beijing, China

 

 

 

Research Interests
Skull base tumor
Cerebrovascular disease
Cranial and cervical junction deformity
Brain Injury

Selected Recent Publications
[1] Sun GC, Chen XL, Hou YZ, Yu XG, Ma XD, Liu G, Liu L, Zhang JS, Tang H, Zhu RY, Zhou DB, Xu BN (2017) Image-guided endoscopic surgery for spontaneous supratentorial intracerebral hematoma. J Neurosurg 127:537-542.
[2] Zhang JS, Qu L, Wang Q, Jin W, Hou YZ, Sun GC, Li FY, Yu XG, Xu BN, Chen XL (2017) Intraoperative visualisation of functional structures facilitates safe frameless stereotactic biopsy in the motor eloquent regions of the brain. Br J Neurosurg doi:10.1080/02688697.2017.1416059.
[3] Yin YH, Qiao GY, Yu XG (2016) Surgical Treatment of Occipitocervical Dislocation with Atlas Assimilation and Klippel-Feil Syndrome Using Occipitalized C1 Lateral Mass and C2 Fixation and Reduction Technique. World Neurosurg 95:46-52.
[4] Yin YH, Tong HY, Qiao GY, Yu XG (2016) Posterior Reduction of Fixed Atlantoaxial Dislocation and Basilar Invagination by Atlantoaxial Facet Joint Release and Fixation: A Modified Technique With 174 Cases. Neurosurgery 78:391-400; discussion 400.
[5] Chen LF, Yang Y, Yu XG, Gui QP, Xu BN, Zhou DB (2015) Multimodal treatment and management strategies for intracranial hemangiopericytoma. J Clin Neurosci 22:718-725. 


 Donald J. Zack, M.D., Ph.D.

 Co-Director, Johns Hopkins Center for Stem Cells and Ocular Regenerative Medicine (STORM)
 Professor of Ophthalmology, Wilmer Eye Institute
 School of Medicine, Johns Hopkins University
 Baltimore, MD, USA

 

 

Background
Donald J. Zack, M.D., Ph.D., is the Guerrieri Professor of Genetic Engineering and Molecular Ophthalmology and co-director of the Center for Stem Cells and Ocular Regenerative Medicine (STORM) at the Wilmer Eye Institute. He is also a professor in the departments of Molecular Biology and Genetics, Neuroscience, and the Institute of Genetic Medicine. His lab studies the control of gene expression in retinal ganglion cells, the cells whose death in glaucoma leads to visual loss and potentially blindness. He also studies the mechanisms by which ganglion cells die in glaucoma, and are developing novel methods to slow down, and hopefully prevent, ganglion cell death in glaucoma. Dr. Zack and his colleagues are beginning studies to promote the differentiation of stem cells into retinal ganglion cells, in the hope that someday that might offer the possibility of restoring vision to glaucoma patients who have already lost significant vision due to ganglion cell death.
Dr. Zack received his M.D. degree and Ph.D. in molecular immunology from the Albert Einstein College of Medicine. After a year of internship, he completed his residency in ophthalmology at the Massachusetts Eye and Ear Infirmary at Harvard University. He then completed fellowship training in glaucoma and molecular biology at the Johns Hopkins University School of Medicine, and joined the faculty in 1991. Dr. Zack has published over 160 peer-reviewed journal articles and has won a number of awards, including the Alcon Research Award.

Selected Recent Publications
[1] Bailey JNC, Gharahkhani P, Kang JH, Butkiewicz M, Sullivan DA, Weinreb RN, Aschard H, Allingham RR, Ashley-Koch A, Lee RK, Moroi SE, Brilliant MH, Wollstein G, Schuman JS, Fingert JH, Budenz DL, Realini T, Gaasterland T, Scott WK, Singh K, et al. (2018) Testosterone Pathway Genetic Polymorphisms in Relation to Primary Open-Angle Glaucoma: An Analysis in Two Large Datasets. Invest Ophthalmol Vis Sci 59:629-636. 
[2] Antony BJ, Carass A, Lang A, Kim BJ, Zack DJ, Prince JL (2017) Longitudinal Analysis of Mouse SDOCT Volumes. Proc SPIE Int Soc Opt Eng 10137. 
[3] Wang X, Maruotti J, Majumdar S, Roman J, Mao HQ, Zack DJ, Elisseeff JH (2017) Collagen vitrigels with low-fibril density enhance human embryonic stem cell-derived retinal pigment epithelial cell maturation. J Tissue Eng Regen Med doi:10.1002/term.2598. 
[4 Sluch VM, Chamling X, Liu MM, Berlinicke CA, Cheng J, Mitchell KL, Welsbie DS, Zack DJ (2017)Enhanced Stem Cell Differentiation and Immunopurification of Genome Engineered Human Retinal Ganglion Cells. Stem Cells Transl Med 6:1972-1986. 
[5] Aschard H, Kang JH, Iglesias AI, Hysi P, Cooke Bailey JN, Khawaja AP, Allingham RR, Ashley-Koch A, Lee RK, Moroi SE, Brilliant MH, Wollstein G, Schuman JS, Fingert JH, Budenz DL, Realini T, Gaasterland T, Scott WK, Singh K, Sit AJ, et al. (2017) Genetic correlations between intraocular pressure, blood pressure and primary open-angle glaucoma: a multi-cohort analysis. Eur J Hum Genet 25:1261-1267.


 Chun-Li Zhang, Ph.D.

 Associate Professor
 Department of Molecular Biology
 Hamon Center for Regenerative Science and Medicine
 University of Texas Southwestern Medical Center
 Dallas, TX, USA

 

 

Biography
Dr. Chun-Li Zhang received his Ph.D. in Genetics and Development from UT Southwestern Medical Center, where he worked on transcriptional control of muscle development and heart disease. Upon graduation in 2003, he conducted postdoctoral research as a HHMI Fellow of the Life Sciences Research Foundation in Dr. Ronald Evans’ laboratory at the Salk Institute, La Jolla, California. In collaboration with Dr. Fred Gage at the same institute, Dr. Zhang worked on adult neural stem cells and neurogenesis. He joined the faculty as an Assistant Professor in 2008 and was promoted to an Associate Professor with tenure in 2014.
The major focus of his laboratory is on molecular and cellular mechanisms controlling adult neural stem cells, neurogenesis, regeneration of the nervous system, and cellular reprogramming for disease modeling and drug identification. Their discoveries were extensively reported by the news media, such as The Scientist Magazine, Nature Reviews Neuroscience, Neurology Today,  The Scientist Magazine, ASL News Today, Healthcanal, Medical News, etc. Their work on reprogramming in vivo was recognized as one of 2014's Big Advances in Science by The Scientist Magazine.

Research Interest
--Genetic and epigenetic regulation of neural stem cells and neurogenesis
--Human neurodegenerative diseases
--Neural regeneration and reprogramming
--Traumatic brain injury and spinal cord injury

Selected Recent Publications
[1] Chen C, Zhong X, Smith DK, Tai W, Yang J, Zou Y, Wang LL, Sun J, Qin S, Zhang CL (2017) Astrocyte-Specific Deletion of Sox2 Promotes Functional Recovery After Traumatic Brain Injury. Cereb Cortex doi:10.1093/cercor/bhx303. 
[2] Wang LL, Su Z, Tai W, Zou Y, Xu XM, Zhang CL (2016) The p53 Pathway Controls SOX2-Mediated Reprogramming in the Adult Mouse Spinal Cord. Cell Rep 17:891-903.
[3] Smith DK, Yang J, Liu ML, Zhang CL (2016) Small Molecules Modulate Chromatin Accessibility to Promote NEUROG2-Mediated Fibroblast-to-Neuron Reprogramming. Stem Cell Reports 7:955-969.
[4] Liu ML, Zang T, Zhang CL (2016) Direct Lineage Reprogramming Reveals Disease-Specific Phenotypes of Motor Neurons from Human ALS Patients. Cell Rep 14:115-128. 
[5] Su Z, Niu W, Liu ML, Zou Y, Zhang CL (2014) In vivo conversion of astrocytes to neurons in the injured adult spinal cord. Nat Commun 5:3338.


 Binhai Zheng, Ph.D.

 Professor
 Department of Neurosciences
 University of California, San Diego
 CA, USA

 

 

Overview
Dr. Zheng’s lab uses genetically modified mice to study why axons in the central nervous system (the brain and the spinal cord) have such a limited ability to regenerate following injury. The insight gained from our research is directly relevant to the design of therapeutic interventions for spinal cord injury, white matter stroke and certain neurodegenerative disorders.

Research Interest
Axon growth, regeneration and repair after CNS injury
Axons in the adult mammalian central nervous system (CNS) have very limited ability to grow and regenerate following injury. Patients of spinal cord injury suffer from permanent functional deficits and paralysis largely because of the poor regenerative ability of CNS axons (for more information on spinal cord injury, click here). Understanding the molecular basis of axon regeneration failure in the CNS will aid in the design of restorative therapies for spinal cord injury, white matter stroke and certain neurodegenerative disorders. Our lab investigates the molecular mechanisms of axonal repair in the CNS by applying a variety of experimental approaches/tools including molecular biology, mouse genetics, viral vectors, in vitro neuronal culture, experimental spinal cord injury, in vivo imaging and CLARITY 3D imaging.

Selected Recent Publications
[1] Meves JM, Zheng B (2016) Synaptic Suppression of Axon Regeneration. Neuron 92:267-269.
[2] Geoffroy CG, Hilton BJ, Tetzlaff W, Zheng B (2016) Evidence for an Age-Dependent Decline in Axon Regeneration in the Adult Mammalian Central Nervous System. Cell Rep 15:238-246.
[3] Lorenzana AO, Lee JK, Mui M, Chang A, Zheng B (2015) A surviving intact branch stabilizes remaining axon architecture after injury as revealed by in vivo imaging in the mouse spinal cord. Neuron 86:947-954.
[4] Geoffroy CG, Lorenzana AO, Kwan JP, Lin K, Ghassemi O, Ma A, Xu N, Creger D, Liu K, He Z, Zheng B (2015) Effects of PTEN and Nogo Codeletion on Corticospinal Axon Sprouting and Regeneration in Mice. J Neurosci 35:6413-6428. 
[5] Chen M, Zheng B (2014) Axon plasticity in the mammalian central nervous system after injury. Trends Neurosci 37:583-593.


 Libing Zhou, Ph.D.

 Professor, Research Director
 Jinan University, China

 

 

 

Overview
Prof. Libing Zhou is currently a neurobiology professor and associate director in Guangdong-Hongkong-Macau Institute for CNS Regeneration. Dr. Zhou obtained MS degree in Human Anatomy & Embryology from Sun Yat-Sen University in 2003 and PhD degree in Neurobiology from University of Catholic Louvain, Belgium in 2008. He worked as a research associate in Institute for Neuroscience, University of Catholic Louvain from 2008 to 2009. In 2009, Dr. Zhou was recruited by Jinan University to establish the Neuroscience Research Team, such as Joint Laboratory of Brain Function and Health, Jinan University and the University of Hong Kong, Guangdong-Hongkong-Macau institute for CNS Regeneration, Guangdong Key Laboratory of Brain Function and Health. His studies mainly focus on key genes in regulating axon guidance and neuronal migration, mechanisms of neural regeneration and repairation, and roles of small molecules in neuronal protection, using knockout and surgical animal models. Dr. Zhou has published many peer review papers in international journals such as Science, J. Neurosci, Nature Neurosci, Cereb Cortex. He was honored as a candidate for “Program for New Century Excellent Talents” in 2009 and for “Guangdong Hundred, Thousand and Ten Talent project” in 2010. Dr. Zhou received more than 10 grants including one 973 Project and two NSFC.

Selected Recent Publications
[1] Lin K, Xu G, Shi L, Lu W, Guan L, Ouyang H, Chen K, Dang Y, Zhou L, So KF (2017) CACNA1C polymorphisms Impact Cognitive Recovery in Patients with Bipolar Disorder in a Six-week Open-label Trial. Sci Rep 7:7022. 
[2] Kang S, Chen X, Gong S, Yu P, Yau S, Su Z, Zhou L, Yu J, Pan G, Shi L (2017) Characteristic analyses of a neural differentiation model from iPSC-derived neuron according to morphology, physiology, and global gene expression pattern. Sci Rep 7:12233. 
[3] Li J, Chen S, Zhao Z, Luo Y, Hou Y, Li H, He L, Zhou L, Wu W (2017) Effect of VEGF on Inflammatory Regulation, Neural Survival, and Functional Improvement in Rats following a Complete Spinal Cord Transection. Front Cell Neurosci 11:381.
[4] Sun X, Jones ZB, Chen XM, Zhou L, So KF, Ren Y (2016) Multiple organ dysfunction and systemic inflammation after spinal cord injury: a complex relationship. J Neuroinflammation 13:260.
[5] Shi L, Guo Y, Dong C, Huddleston J, Yang H, Han X, Fu A, Li Q, Li N, Gong S, Lintner KE, Ding Q, Wang Z, Hu J, Wang D, Wang F, Wang L, Lyon GJ, Guan Y, Shen Y, Evgrafov OV, Knowles JA, Thibaud-Nissen F, Schneider V, Yu CY, Zhou L, Eichler EE, So KF, Wang K (2016) Long-read sequencing and de novo assembly of a Chinese genome. Nat Commun 7:12065.


 Hui Zhu, Ph.D.

 Director
 All-Military Spinal Cord Injury Treatment Centre
 Kunming Tongren Hospital,
 Kunming, Yunnan Province, China

 

 

Overview
Dr Zhu Hui is founder and first director of the All-Military Spinal Cord Injury Treatment Centre.  She is a member of numerous academic committees on spinal cord injury research both in China and abroad and has chaired international, national, national, provincial and military research projects on various topics related to spinal cord injury. She has been the second place winner of the National Science and Technology Progress Award, second place winner of the Military Award for Medical Achievement and first place winner of the Yunnan Province Science and Technology Progress Award. She has been the recipient of the Grant for Outstanding Professionals in the Military for her contributions to improving diagnosis and treatment of spinal cord injury, disability assessment, rehabilitation training (development of the Kunming Walking Method and the Kunming Locomotor Scale) and perisurgical care and treatment of complications in spinal cord injury.


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