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Integrative Physiology & Pharmacology Ph.D. Program at Wake Forest University


Wake Forest University Graduate School » Integrative Physiology & Pharmacology Ph.D. Program

Tao Ma

Tao Ma
Ma T, Liu S, Zhang WL, Zhao H, Yu SY, He RR. (2002) Electrophysiological effects of phytoestrogen genistein on human atrial fibers. Acta Pharmacol Sin. 23:851-854. PMID: 12230957   Tsokas P, Grace EA, Chan P, Ma T, Sealfon SC, Iyengar R, Landau EM, Blitzer RD (2005) Local protein synthesis mediates a rapid increase in dendritic elongation factor 1A after induction of late long-term potentiation. J Neurosci 25:5833-5843. PMID: 15958750.   Tsokas P*, Ma T*, Iyengar R, Landau EM, Blitzer RD (2007) Mitogen-activated protein kinase upregulates the dendritic translation machinery in long-term potentiation by controlling the mammalian target of rapamycin pathway. J Neurosci 27: 5885 - 5894 (* equal contribution, co-first author). PMID: 17537959.   Tampellini D, Rahman N, Gallo EF, Huang Z, Dumont M, Capetillo-Zarate E, Ma T, Zheng R, Lu B, Nanus DM, Lin MT, Gouras GK (2009) Synaptic activity reduces intraneuronal Abeta, promotes APP transport to synapses, and protects against Abeta-related synaptic alterations. J Neurosci 29:9704-9713. PMID: 19657023; PMCID: PMC2763626   Ma T, Hoeffer CA, Capetillo-Zarate E, Yu F, Wong H, Lin MT, Tampellini D, Klann E, Blitzer RD, Gouras GK (2010) Dysregulation of the mTOR pathway mediates impairment of synaptic plasticity in a mouse model of Alzheimer's disease. PLoS One. 5. pii: e12845. PMID: 20862226; PMCID: PMC2942840   Ma T*, Hoeffer CA*, Wong H, Massaad CA, Zhou P, Iadecola C, Murphy MP, Paulter RG, Klann E (2011) Amyloid beta-induced Impairments in hippocampal synaptic plasticity are rescued by decreasing mitochondrial superoxide. J Neurosci 31: 5589-5595 (paper of the week * equal contribution, co-first author). PMID: 21490199; PMCID: PMC3095121   Ma T, Tzavaras N, Tsokas P, Landau EM, Blitzer RD (2011) Synaptic stimulation of mTOR is mediated by Wnt signaling and regulation of glycogen synthetase kinase-3. J Neurosci 31: 17537-17546 (cover paper). PMID: 22131415.   Ma T and Klann E (2012) Amyloid β: linking synaptic plasticity failure to memory disruption in Alzheimer’s Disease. J Neurochem 120 Suppl 1: 140-148. PMID: 22122128. PMCID: PMC3254830.   Ma T, Du X, Pick J, Sui G, Brownlee M, Klann E (2012) Glucagon-like peptide-1 cleavage product GLP-1 (9-36) amide rescues synaptic plasticity and memory deficits in Alzheimer's Disease model mice. J Neurosci. 32: 13701-13708 (paper of the week). PMID: 23035082. PMCID: PMC3475870.   Ma T, Trinh MA, Wexler AJ, Bourbon C, Gatti E, Pierre P, Cavener DR, Klann E (2013) Suppression of PERK-eIF2α signaling alleviates synaptic plasticity and spatial memory deficits in Alzheimer's disease model mice. Nat Neurosci. 16:1299-1305. PMID: 23933749. PMCID: PMC3756900.   Hoeffer CA, Santini E, Ma T, Arnold E, Whelan A, Wong H, Pierre P, Pelletier J, Klann E (2012) Multiple components of eIF4F are required for protein synthesis-dependent hippocampal long-term potentiation. J Neurophysiol 109:68-76. PMID: 23054596. PMCID: PMC3545154   Ma T (2014) GSK3 in Alzheimer’s Disease – Mind the Isoforms. J Alzheimers Dis. 39:707-710. PMID:24254703. PMCID: pending.   Kurinami H, Shimamura M, Ma T, Liping Qian, Kenzo Koizumi, Laibaik Park, Eric Klann, Giovanni Manfredi, Costantino Iadecola, Ping Zhou (2014) Prohibitin viral gene transfer protects hippocampal CA1 neurons from ischemia-reperfusion and rescues hippocampal function . Stroke. 45:1131-1138. PMID: 24619393. PMCID: PMC3971834.   Trinh MA*, Ma T*, Kaphzan H, Bhattacharya A, Antion MD, Cavener DR, Hoeffer CA, Klann E (2014) The eIF2α kinase PERK limits the expression of hippocampal metabotropic glutamate receptor-dependent long-term depression. Learn Mem. 21:298-304. (*equal contribution, co-first author). PMID: 24741110. PMCID: PMC 3994503.   Ma T, Chen Y, Vingtdeux V, Zhao H, Viollet B, Marambaud P, Klann E (2014) Inhibition of AMP-activated protein kinase signaling alleviates impairments in hippocampal synaptic plasticity induced by amyloid β. J Neurosci 34: 12230-12238 (paper of the week). PMID: 25186765. PMCID: PMC4152616.

 

Dr. Ma received his MD in China and his PhD in Neuroscience from Mount Sinai School of Medicine at New York in 2008, working with Drs. Robert Blitzer and Emmanuel Landau. From 2008-2010, he was a postdoctoral research fellow with Dr. Gunnar Gouras in the Department of Neurology and Neuroscience at Weill Cornell Medical College of Cornell University. From 2010 and 2014, he was an Assistant Research Scientist followed by Research Assistant Professor at the New York University Center for Neural Science, laboratory of Dr. Eric Klann. Since 2014, Dr. Ma has been a tenure-track assistant professor at Wake Forest University School of Medicine (NC, USA), Department of Internal Medicine-Gerontology and Geriatric Medicine.   Dr. Ma is a neuroscientist with specialization in learning, memory, and synaptic plasticity. His research focuses on novel molecular mechanisms underlying pathophysiology of Alzheimer’s disease (AD) and subsequently to identify potential therapeutic targets or biomarkers for AD and other aging-related cognitive impairments. Primary techniques applied in his laboratory include electrophysiology, confocal microscopy, behavioral tests, and molecular approaches in transgenic mouse models. His original research findings on molecular mechanisms in AD have been published in many high-profile peer-reviewed journals including “The journal of Neuroscience” and “Nature Neuroscience”, and garnered international attention.   Dr. Ma has won numerous awards. He is a recipient and principal investigator of National Institute of Health/National Institute of Aging K99/R00 research grant. He also serves as principal investigator of a research grant from the BrightFocus Foundation. He has been an editor of “International Journal of Neurology Research”, and associate editor of “Journal of Alzheimer’s Disease”. He is a member of “Society for Neuroscience” and “New York Academy of Science”.

 

The focus of my laboratory is to investigate novel molecular mechanisms underlying pathogenesis of Alzheimer’s disease (AD) and subsequently identify potential therapeutic targets or biomarkers for AD and other aging-related cognitive impairments. I have a broad background in neuroscience, with specific training and expertise in key research areas for this application. I started scientific research as a medical student and later a master student majoring in physiology at Hebei Medical University in China. My research work as a PhD student at Mount Sinai School of Medicine in New York revealed novel signaling mechanisms underlying synaptic plasticity, learning and memory, leading to two featured publications at “The Journal of Neuroscience”. As postdoctoral researcher at Cornell Medical College and New York University, I have focused my study on the cellular/molecular mechanisms underlying Alzheimer’s disease, and importantly, translation of these mechanisms into therapeutics. During this period, I have obtained interesting findings regarding the role of protein synthesis, mitochondrial reactive oxygen species, and cellular metabolisms in AD pathophysiology, result into a number of publications in high-impact peer-reviewed journals.  Since 2014, I have joined Wake Forest School of Medicine as a tenure-track assistant professor. Multiple experimental approaches are used in my laboratory to achieve a greater understanding of cellular/molecular mechanisms and potential novel therapeutic avenues for AD and other cognitive defects. Primary techniques include molecular biology, confocal microscopy, electrophysiology, behavioral analysis in genetic altered mice etc. With my research background and the tremendous support from Wake Forest School of Medicine, I believe that I have the expertise, resources, leadership, and motivation necessary to successfully fulfil the proposed role in this application.