Bio

Dr. Wang is a board-certified, fellowship-trained neurocritical care specialist at Stanford Health Care. He is also an instructor in the Neurocritical Care Program of the Department of Neurology & Neurological Sciences at Stanford University School of Medicine.

Dr. Wang has clinical and research interests in stroke and traumatic brain injury. He provides care for critically ill patients with neurological illnesses in the intensive care unit (ICU) at Stanford Hospital. He also teaches fellows, residents, and medical students how to provide critical neurological care.

As a physician-scientist, Dr. Wang leads an ongoing effort to identify new targets for therapy to promote functional recovery after brain and spinal cord injuries. He has previously completed research on these topics for the National Institutes of Health (NIH) and the National Institute of Neurological Disorders and Stroke (NINDS). He also performs research funded by the American Heart Association, American Academy of Neurology, and Alzheimer’s Association.

Dr. Wang has published in several top peer-reviewed journals, including Proceedings of the National Academy of Sciences, Journal of Cell Biology, and Journal of Neuroscience. He has presented his research at nationwide and worldwide conferences. His presentations mainly focus on the degeneration of axons (fibers that connect nerve cells and help them communicate) and cognitive decline following stroke. He also serves as an ad hoc reviewer for a number of publications, including Cell, Neuron, Nature, and Science.

Dr. Wang is a member of the American Academy of Neurology, American Heart Association, Neurocritical Care Society, Society of Critical Care Medicine, and Society for Neuroscience.

Clinical Focus

  • Neurocritical Care

Academic Appointments

Honors & Awards

  • Clinician Scientist Early Career Award, Alzheimer's Association (2024)
  • Career Development Award, American Academy of Neurology (2023)
  • Career Development Award, American Heart/Stroke Association (2023)
  • NCS Research Fellowship, Neurocritical Care Society (2022-2023)
  • StrokeNet Research Fellowship, NINDS (2020-2021)
  • Semel Institute Neuroscience Research Award, UCLA-Semel Neuroscience Institute (2018)
  • Excellence in Research, Los Angeles Neurological Society (2018)
  • R25 Research Training Fellowship, NINDS (2016-2020)
  • Bio-X Bowes Fellow, Stanford University School of Medicine (2011-2014)
  • Predoctoral Research Fellowship, American Heart/Stroke Association (2009-2011)
  • Translational Research Scholar, Adelson Neural Repair & Rehabilitation Foundation (2008-2011)
  • Delegate, International Achievement Summit (2007)
  • Predoctoral Medical Research Fellowship, Howard Hughes Medical Institute (2005-2007)
  • Excellence in Undergraduate Teaching, Stanford University, Department of Biological Sciences (2003)

Professional Education

  • Board Certification: American Board of Psychiatry and Neurology, Neurocritical Care (2021)
  • Board Certification: American Board of Psychiatry and Neurology, Vascular Neurology (2020)
  • Board Certification: American Board of Psychiatry and Neurology, Neurology (2018)
  • Fellowship: Stanford University Neurocritical Care and Stroke Fellowship (2020) CA
  • Residency: UCLA Dept of Neurology (2018) CA
  • Internship: Kaiser Permanente Santa Clara Internal Medicine Residency (2015) CA
  • Medical Education: Stanford University School of Medicine (2014) CA
  • PhD, Stanford University School of Medicine, Neuroscience (2014)
  • MD, Stanford University School of Medicine, Medicine (2014)

Contact

  • Academic
    jtw@stanford.edu
    University - Other Teaching/Research Department: Adult Neurology Position: Instructor
    • Center for Academic Medicine
    • Stanford Stroke Center
    • 453 Quarry Road, Mail Code 5235
    • Stanford,  California  94304 
  • Clinical (Primary)  Stanford Neurosurgery Dept 453 Quarry Rd Ste 245 MC 5327 Palo Alto, CA 94304 (650) 723-4451 (fax)

Additional Clinical Info

Links

Current Research and Scholarly Interests

Our primary research focus is understanding the molecular mechanisms of axonal degeneration and subsequent failure of axonal regeneration in the CNS. We have identified critical cellular pathways mediating axonal degeneration following acute neurological injuries including ischemic stroke and traumatic brain injury. Modulating these pathways presents a novel therapeutic strategy to protect vulnerable nerve fibers and enhance functional recovery in a multitude of acute CNS injuries and diseases.

2024-25 Courses

All Publications

  • What are the Molecular Mechanisms of Axonal Degeneration in Stroke? Wang, J. LIPPINCOTT WILLIAMS & WILKINS. 2021

    View details for Web of Science ID 000729283605325

  • Absence of Sarm1 Promotes Axonal and Neuronal Survival after Stroke Wang, J., Toh, B., Komuro, Y., Hinman, J. D. WILEY. 2019: S240

    View details for Web of Science ID 000488891800460

  • Developmental mechanisms for establishing functional non-image-forming visual circuits Dhande, O. S., Phan, A. H., Seabrook, T. A., Nguyen, P. L., Wang, J. T., Huberman, A. ASSOC RESEARCH VISION OPHTHALMOLOGY INC. 2017

    View details for Web of Science ID 000432170304131

  • Local axonal protection by WldS as revealed by conditional regulation of protein stability PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Wang, J. T., Medress, Z. A., Vargas, M. E., Barres, B. A. 2015; 112 (33): 10093-10100

    Abstract

    The expression of the mutant Wallerian degeneration slow (WldS) protein significantly delays axonal degeneration from various nerve injuries and in multiple species; however, the mechanism for its axonal protective property remains unclear. Although WldS is localized predominantly in the nucleus, it also is present in a smaller axonal pool, leading to conflicting models to account for the WldS fraction necessary for axonal protection. To identify where WldS activity is required to delay axonal degeneration, we adopted a method to alter the temporal expression of WldS protein in neurons by chemically regulating its protein stability. We demonstrate that continuous WldS activity in the axonal compartment is both necessary and sufficient to delay axonal degeneration. Furthermore, by specifically increasing axonal WldS expression postaxotomy, we reveal a critical period of 4-5 h postinjury during which the course of Wallerian axonal degeneration can be halted. Finally, we show that NAD(+), the metabolite of WldS/nicotinamide mononucleotide adenylyltransferase enzymatic activity, is sufficient and specific to confer WldS-like axon protection and is a likely molecular mediator of WldS axon protection. The results delineate a therapeutic window in which the course of Wallerian degeneration can be delayed even after injures have occurred and help narrow the molecular targets of WldS activity to events within the axonal compartment.

    View details for DOI 10.1073/pnas.1508337112

    View details for Web of Science ID 000359738300028

    View details for PubMedCentralID PMC4547231

  • Gap junctions are essential for generating the correlated spike activity of neighboring retinal ganglion cells. PloS one Völgyi, B., Pan, F., Paul, D. L., Wang, J. T., Huberman, A. D., Bloomfield, S. A. 2013; 8 (7): e69426

    Abstract

    Neurons throughout the brain show spike activity that is temporally correlated to that expressed by their neighbors, yet the generating mechanism(s) remains unclear. In the retina, ganglion cells (GCs) show robust, concerted spiking that shapes the information transmitted to central targets. Here we report the synaptic circuits responsible for generating the different types of concerted spiking of GC neighbors in the mouse retina. The most precise concerted spiking was generated by reciprocal electrical coupling of GC neighbors via gap junctions, whereas indirect electrical coupling to a common cohort of amacrine cells generated the correlated activity with medium precision. In contrast, the correlated spiking with the lowest temporal precision was produced by shared synaptic inputs carrying photoreceptor noise. Overall, our results demonstrate that different synaptic circuits generate the discrete types of GC correlated activity. Moreover, our findings expand our understanding of the roles of gap junctions in the retina, showing that they are essential for generating all forms of concerted GC activity transmitted to central brain targets.

    View details for DOI 10.1371/journal.pone.0069426

    View details for PubMedID 23936012

    View details for PubMedCentralID PMC3720567

  • Gap Junctions Are Essential for Generating the Correlated Spike Activity of Neighboring Retinal Ganglion Cells PLOS ONE Voelgyi, B., Pan, F., Paul, D. L., Wang, J. T., Huberman, A. D., Bloomfield, S. A. 2013; 8 (7)

    Abstract

    Neurons throughout the brain show spike activity that is temporally correlated to that expressed by their neighbors, yet the generating mechanism(s) remains unclear. In the retina, ganglion cells (GCs) show robust, concerted spiking that shapes the information transmitted to central targets. Here we report the synaptic circuits responsible for generating the different types of concerted spiking of GC neighbors in the mouse retina. The most precise concerted spiking was generated by reciprocal electrical coupling of GC neighbors via gap junctions, whereas indirect electrical coupling to a common cohort of amacrine cells generated the correlated activity with medium precision. In contrast, the correlated spiking with the lowest temporal precision was produced by shared synaptic inputs carrying photoreceptor noise. Overall, our results demonstrate that different synaptic circuits generate the discrete types of GC correlated activity. Moreover, our findings expand our understanding of the roles of gap junctions in the retina, showing that they are essential for generating all forms of concerted GC activity transmitted to central brain targets.

    View details for DOI 10.1371/journal.pone.0069426

    View details for Web of Science ID 000325211000118

    View details for PubMedCentralID PMC3720567

  • Culturing hybridoma cell lines for monoclonal antibody production. Cold Spring Harbor protocols Winzeler, A., Wang, J. T. 2013; 2013 (7): 640-642

    Abstract

    This protocol describes how to culture hybridoma cell lines (e.g., Thy1.1) for monoclonal antibody production. Supernatants harvested from such cultures can be used to purify various rodent neural cell types by immunopanning.

    View details for DOI 10.1101/pdb.prot074914

    View details for PubMedID 23818668

  • Purification and culture of retinal ganglion cells. Cold Spring Harbor protocols Winzeler, A., Wang, J. T. 2013; 2013 (7): 614-617

    Abstract

    Retinal ganglion cells (RGCs) are the neurons that extend axons through the optic nerve, connecting and transmitting information from the retina to the brain. In mammals, RGCs receive information from bipolar and amacrine cells and synapse onto target cells in the lateral geniculate nucleus (LGN) as well as the superior colliculus. Methods for acute purification of RGCs from rodent retina by immunopanning followed by culture in a serum-free medium have facilitated the study of neuronal biology and function in a defined environment. These methods are introduced here, and modifications for achieving optimal RGC purity and culture are described.

    View details for DOI 10.1101/pdb.top070961

    View details for PubMedID 23818663

  • Purification and culture of retinal ganglion cells from rodents. Cold Spring Harbor protocols Winzeler, A., Wang, J. T. 2013; 2013 (7): 643-652

    Abstract

    Here we describe methods for acute purification of retinal ganglion cells (RGCs) from rodent retina by immunopanning, followed by culture in serum-free medium. Though the method was initially established and verified with rats, we have included modifications for the purification of mouse RGCs. This protocol is written for isolation of cells from one litter of pups. All of the volumes and numbers of panning plates should be scaled according to the number of litters used, particularly for rat RGCs.

    View details for DOI 10.1101/pdb.prot074906

    View details for PubMedID 23818667

  • Axon Degeneration: Where the Wld(s) Things Are CURRENT BIOLOGY Wang, J. T., Barres, B. A. 2012; 22 (7): R221-R223

    Abstract

    Expression of the Wld(s) protein significantly delays axon degeneration in injuries and diseases, but the mechanism for this protection is unknown. Two recent reports present evidence that axonal mitochondria are required for Wld(S)-mediated axon protection.

    View details for DOI 10.1016/j.cub.2012.02.056

    View details for Web of Science ID 000302844900006

    View details for PubMedID 22497934

  • Axon degeneration: Molecular mechanisms of a self-destruction pathway JOURNAL OF CELL BIOLOGY Wang, J. T., Medress, Z. A., Barres, B. A. 2012; 196 (1): 7-18

    Abstract

    Axon degeneration is a characteristic event in many neurodegenerative conditions including stroke, glaucoma, and motor neuropathies. However, the molecular pathways that regulate this process remain unclear. Axon loss in chronic neurodegenerative diseases share many morphological features with those in acute injuries, and expression of the Wallerian degeneration slow (WldS) transgene delays nerve degeneration in both events, indicating a common mechanism of axonal self-destruction in traumatic injuries and degenerative diseases. A proposed model of axon degeneration is that nerve insults lead to impaired delivery or expression of a local axonal survival factor, which results in increased intra-axonal calcium levels and calcium-dependent cytoskeletal breakdown.

    View details for DOI 10.1083/jcb.201108111

    View details for Web of Science ID 000299269000003

    View details for PubMedID 22232700

    View details for PubMedCentralID PMC3255986

  • Disease gene candidates revealed by expression profiling of retinal ganglion cell development JOURNAL OF NEUROSCIENCE Wang, J. T., Kunzevitzky, N. J., Dugas, J. C., Cameron, M., Barres, B. A., Goldberg, J. L. 2007; 27 (32): 8593-8603

    Abstract

    To what extent do postmitotic neurons regulate gene expression during development or after injury? We took advantage of our ability to highly purify retinal ganglion cells (RGCs) to profile their pattern of gene expression at 13 ages from embryonic day 17 through postnatal day 21. We found that a large proportion of RGC genes are regulated dramatically throughout their postmitotic development, although the genes regulated through development in vivo generally are not regulated similarly by RGCs allowed to age in vitro. Interestingly, we found that genes regulated by developing RGCs are not generally correlated with genes regulated in RGCs stimulated to regenerate their axons. We unexpectedly found three genes associated with glaucoma, optineurin, cochlin, and CYP1B1 (cytochrome P450, family 1, subfamily B, polypeptide 1), previously thought to be primarily expressed in the trabecular meshwork, which are highly expressed by RGCs and regulated through their development. We also identified several other RGC genes that are encoded by loci linked to glaucoma. The expression of glaucoma-linked genes by RGCs suggests that, at least in some cases, RGCs may be directly involved in glaucoma pathogenesis rather than indirectly involved in response to increased intraocular pressure. Consistent with this hypothesis, we found that CYP1B1 overexpression potentiates RGC survival.

    View details for DOI 10.1523/JNEUROSCI.4488-07.2007

    View details for Web of Science ID 000248708400013

    View details for PubMedID 17687037

    View details for PubMedCentralID PMC2885852

  • An oligodendrocyte lineage-specific semaphorin, sema5A, inhibits axon growth by retinal ganglion cells JOURNAL OF NEUROSCIENCE Goldberg, J. L., Vargas, M. E., Wang, J. T., Mandemakers, W., Oster, S. F., Sretavan, D. W., Barres, B. A. 2004; 24 (21): 4989-4999

    Abstract

    In the mammalian CNS, glial cells repel axons during development and inhibit axon regeneration after injury. It is unknown whether the same repulsive axon guidance molecules expressed by glia and their precursors during development also play a role in inhibiting regeneration in the injured CNS. Here we investigate whether optic nerve glial cells express semaphorin family members and, if so, whether these semaphorins inhibit axon growth by retinal ganglion cells (RGCs). We show that each optic nerve glial cell type, astrocytes, oligodendrocytes, and their precursor cells, expressed a distinct complement of semaphorins. One of these, sema5A, was expressed only by purified oligodendrocytes and their precursors, but not by astrocytes, and was present in both normal and axotomized optic nerve but not in peripheral nerves. Sema5A induced collapse of RGC growth cones and inhibited RGC axon growth when presented as a substrate in vitro. To determine whether sema5A might contribute to inhibition of axon growth after injury, we studied the ability of RGCs to extend axons when cultured on postnatal day (P) 4, P8, and adult optic nerve explants and found that axon growth was strongly inhibited. Blocking sema5A using a neutralizing antibody significantly increased RGC axon growth on these optic nerve explants. These data support the hypothesis that sema5A expression by oligodendrocyte lineage cells contributes to the glial cues that inhibit CNS regeneration.

    View details for DOI 10.1523/JNEUROSCI.4390-03.2004

    View details for Web of Science ID 000221654400011

    View details for PubMedID 15163691