Lee A. Shapiro, PhD

Associate Professor

Contact

Department of Neuroscience & Experimental Therapeutics
8447 Riverside Pkwy
2006 Medical Research and Education Building
Bryan, TX 77807
lshapiro@tamu.edu
Phone: 979.436.0272
Fax: 979.436.0086

Biography

Dr. Shapiro received his PhD in neuroscience from the State University of New York, Stony Brook, under the mentorship of Dr. Patricia Whitker-Azmitia. His dissertation involved looking at serotonergic, neuroimmune and neuropathological influences in Down Syndrome and Alzheimer's disease, specifically focusing on the role of S100 beta. After receiving his PhD, Dr. Shapiro went to the University of California, Irvine, to do post-doctoral research under the guidance of Dr. Charles Ribak. Dr. Shapiro honed his neuroanatomical and microscopy skills under the guidance of Dr. Ribak, while describing neuronal and glial changes in models of epilepsy. During his post-doctoral studies, Dr. Shapiro also pioneered several unique aspects of adult neurogenesis in the hippocampus, and in other cortical regions. After completing his Fellowship, Dr. Shapiro came to Texas A&M University and established his own lab as described below, and is further pursuing studies involving epilepsy, trauma and other neurodegenerative disorders.

Research Interests

My lab focuses on neuroanatomical, neuropathological, neuroimmune and peripheral contributions to traumatic brain injury (TBI), epilepsy, Alzheimer’s Disease, and other neurodegenerative disorders. In this context, we use advanced microscopic and other imaging techniques to assess the efficacy of immune and neuroimmune therapeutic strategies, on neurobehavioral outcomes, including depression and cognitive impairment, both of which are hallmarks of TBI and Alzheimer’s disease. We also examine endogenous stem cells and their response to TBI and potential beneficial and pathological effects of these stem cells. To further enhance our ability to identify and therapeutically target potential disease mechanisms, we incorporate electrophysiological strategies for our investigations. We have identified numerous novel pathogenic mechanisms and have published extensively on these topics.
Because about 3 million people experience a TBI in the United States each year, and because TBI leads to a 2.3-4.5-fold increase in the likelihood of developing Alzheimer’s disease, a major focus of the lab is to elucidate therapeutic mechanisms that can be targeted to prevent the development of Alzheimer’s disease. There are many immune, neuroimmune and neuroanatomical similarities between TBI and Alzheimer’s disease and elucidating dual targets for both disorders is a major goal of my lab. Importantly, it is becoming very clear that organ systems outside of the brain, namely the gastrointestinal system, are involved in the pathogenic processes of TBI and Alzheimer’s disease. Thus, an area of our research focuses specifically on the gut and gut/brain/immune interactions to identify novel therapeutic strategies.
We also use epilepsy and post-traumatic epilepsy models to examine changes in the brain that contribute to the development of seizures and epilepsy after precipitating brain or immune insults. My lab also utilizes models of military illness to assess similar links to neuroimmune, peripheral immune and peripheral organ contributions. Finally, my lab is intensively involved in exploring and elucidating the peripheral/brain axis, and how the brain and body interact to improve or exacerbate outcome measures. These studies include the gut, but also other peripheral organs such as the spleen, the heart, the lungs, and the lymphatic system.
I am committed to training the next generation of scientists, through undergraduate. Graduate, medical, and postdoctoral programs.
Research in my lab is supported by the National Institute of Neurological Disorders and Stroke (NINDS), the Congressionally Directed Medical Research programs, the United States Army Medical Research and Development Command (USAMRDC), the Department of Defense (DOD) Peer-Reviewed Alzheimer’s Research Program, the DOD Toxic Exposures Research program, and generous support from the Woodnext Foundation.

Representative Publications

Arisi GM, Foresti ML, Katki K, Shapiro LA (2015). Increased CCL2, CCL3, CCL5, and IL-1β cytokine concentration in piriform cortex, hippocampus, and neocortex after pilocarpine-induced seizures. J Neuroinflammation. 2;12:129.
Robinson C, Apgar C, Shapiro LA (2016). Astrocyte hypertrophy contributes to aberrant neurogenesis after traumatic brain injury. Neural Plasticity, in press.
Wang F*, Wang X*, Shapiro LA &*, Cotrina ML, Liu W, Wang EW, Gu S, Wang W, He X, Nedergaard M, Huang JH (2016). NKCC1 up-regulation contributes to early post-traumatic seizures and increased post-traumatic seizure susceptibility; &Co-first Author,*Co-corresponding Authors.
Nizamutdinov D, DeMorrow S, McMillian M, Kain J, Mukherjee S, Zeitouni S, Frampton G, Bricker PC, Hurst J, Shapiro LA (2017). Bile acid system alterations in the hypothalamus and liver are accompanied by hepatic changes after traumatic brain injury. Scientific Report; 2017 Jan 20;7:40112. doi:10.1038/srep40112.
Overview of Traumatic Brain Injury: An Immunological Context. Nizamutdinov D, Shapiro LA (2016). Brain Sci. 2017 Jan 23;7(1).
Stress Induced Neuroplasticity and Mental Disorders (2017). Wang F, Pan F, Shapiro LA, Huang JH. Neural Plast. 2017;2017:9634501.
Altered Hippocampal Neurogenesis during the First 7 Days after a Fluid Percussion Traumatic Brain Injury (2017). Shapiro LA. Cell Transplant. 2017 Jul;26(7):1314-1318.