Projects per year
Personal profile
Personal profile
During her postdoctoral training, Dr. Zhao conducted research on amyotrophic lateral sclerosis (ALS) or Lou Gehrig’s disease. She investigated the roles of glutamate-mediated cytotoxicity, immune-mediated injury, and oxidative stress in motor neuron death. She also investigated the potential for a new phospholipid agent, VP025, to inhibit immune activation and protect motor neurons from injury. After completing her postdoctoral fellowship, Dr. Zhao joined the Methodist Hospital Research Institute as a scientist in the Department of Neurology.
Research interests
Research interests
Amyotrophic lateral sclerosis (ALS), commonly known as Lou Gehrig’s disease, is a progressive neurodegenerative disease that attacks motor neurons in the brain and spinal cord. Dr. Zhao is interested in the underlying mechanisms of neuroinflammation on motor neuron death and relevant therapeutic targets. Current research efforts aim to understand the roles of microglia/monocytes and T-cells on immune-mediated injury and repair in ALS. Dr. Zhao is investigating the neuroprotective potential of regulatory immune cells as new therapeutic options for ALS. Gene mutations on SOD1, TDP-43, and C9ORF72 have been linked to ALS. Dr. Zhao is also interested in the pathology of various mutant proteins as well as abnormal peptides, and how they affect interactions among motor neurons, microglia, and T-cells in ALS.
Education/Academic qualification
Neurology, Postdoctoral Fellowship, Baylor College of Medicine
Neurology, MD, Beijing Medical University, Beijing
Neurology, PhD, Peking University
Free-text keywords
- ALS
- Lou Gehrig’s disease
- Immune Suppression
- Inflammation
- Neuroprotection
- Neurocytotoxicity
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Recent external collaboration on country/territory level. Dive into details by clicking on the dots or
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Immune Mechanisms in Amyotrophic Lateral Sclerosis
Appel, S. H., Beers, D. & Zhao, W.
Muscular Dystrophy Association
5/1/14 → 4/30/17
Project: Non Profit
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Blocking TLR-Activation of Regulatory T cells Slows Disease in ALS
Appel, S. H., Beers, D. & Zhao, W.
Natl Inst of Neuro Disorders and Stroke
3/15/13 → 8/31/15
Project: Federal Funding Agencies
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CD4+CD25+ Treg cell regulate microglia and provide neuroprotection in ALS
Natl Inst of Neuro Disorders and Stroke
5/1/10 → 3/31/13
Project: Federal Funding Agencies
Research output
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Combined Regulatory T-Lymphocyte and IL-2 Treatment Is Safe, Tolerable, and Biologically Active for 1 Year in Persons With Amyotrophic Lateral Sclerosis
Thonhoff, J. R., Berry, J. D., Macklin, E. A., Beers, D. R., Mendoza, P. A., Zhao, W., Thome, A. D., Triolo, F., Moon, J. J., Paganoni, S., Cudkowicz, M. & Appel, S. H., Nov 1 2022, In: Neurology(R) neuroimmunology & neuroinflammation. 9, 6Research output: Contribution to journal › Article › peer-review
Open Access -
Extracellular Vesicles Derived From Ex Vivo Expanded Regulatory T Cells Modulate In Vitro and In Vivo Inflammation
Thome, A. D., Thonhoff, J. R., Zhao, W., Faridar, A., Wang, J., Beers, D. R. & Appel, S. H., Jun 22 2022, In: Frontiers in immunology. 13, 875825.Research output: Contribution to journal › Article › peer-review
Open Access -
Tregs Attenuate Peripheral Oxidative Stress and Acute Phase Proteins in ALS
Beers, D. R., Thonhoff, J. R., Faridar, A., Thome, A. D., Zhao, W., Wen, S. & Appel, S. H., Aug 2022, In: Annals of Neurology. 92, 2, p. 195-200 6 p.Research output: Contribution to journal › Article › peer-review
Open Access -
Amyotrophic lateral sclerosis is a systemic disease: peripheral contributions to inflammation-mediated neurodegeneration
Appel, S. H., Beers, D. R. & Zhao, W., Oct 1 2021, In: Current opinion in neurology. 34, 5, p. 765-772 8 p.Research output: Contribution to journal › Review article › peer-review
7 Scopus citations -
Ex vivo expansion of dysfunctional regulatory T lymphocytes restores suppressive function in Parkinson’s disease
Thome, A. D., Atassi, F., Wang, J., Faridar, A., Zhao, W., Thonhoff, J. R., Beers, D. R., Lai, E. C. & Appel, S. H., Dec 2021, In: npj Parkinson's Disease. 7, 1, 41.Research output: Contribution to journal › Article › peer-review
Open Access8 Scopus citations