Research Abstract:
I have two primary lines of research within the domains of clinical and cognitive neuroscience/neuropsychology. One focuses on the neural underpinnings of cognitive dysfunction in diseases relevant to dopamine and the basal ganglia (e.g. Parkinson’s disease (PD) and Tourette Syndrome (TS)). The other focuses on the effects of developmental metabolic insults on cognitive function and the brain in children with diabetes. Both use a novel combination of techniques and have the potential to answer important question relevant to human diseases and their impact on the brain, cognitive function, mood and development.
1) Pathophysiology of basal ganglia-thalamocortical (BG-TH-CTX) pathways. Many diseases with known or suspected dysfunction of the BG-TH-CTX pathways (e.g. PD, TS, Huntington’s disease, Attention deficit disorder, etc.) are characterized by motor, mood and cognitive dysfunction. However, our current understanding of how these very different disease states can affect the similar anatomical pathways to produce qualitatively different behavioral dysfunction is very limited. Our overall goal is to determine how disease states such as PD and TS affect these pathways to produce mood and cognitive dysfunction. We reason that dysfunction should be more evident when these pathways are engaged or challenged. Thus, we use neuroimaging techniques to test hypotheses about how the function of these pathways responds to dopaminergic, electrical and cognitive challenges.
2) Cognitive neuroscience of diabetes: Our understanding of the effects of developmental metabolic insults on cognitive function and the brain in humans is currently very limited. Using neuroimaging techniques (structural MRI, diffusion tensor imaging, functional MRI) and a large, prospectively assessed cohort of youth with and without type 1 diabetes (T1DM), we are testing hypotheses about how glycemic extremes, brain structural integrity and cognitive function are related in youth with T1DM. Ultimately, these data will help determine whether central nervous system structure and function should join the peripheral nervous system, retina and kidneys as systems at risk during development in T1DM. This knowledge would have significant clinical implications for the optimal care of youth with T1DM as well as for our understanding of how the developmental trajectory of the brain can be altered by metabolic extremes.
Selected Publications:
Campbell MC, Karimi M, Videen TO, Weaver PM, Tabbal SD, Perlmutter JS, HersheyT. Neural correlates of STN DBS-induced impairment in cognitive function. Neuropsychologia 2008 48(13): 3162-9.
Foster ER, McDaniel MA, Repovs G, Hershey T. Prospective memory in Parkinson disease across laboratory and self-reported everyday performance. Neuropsychology 2009 23(3): 347-58
Foster ER, Black KJ, Antenor-Dorsey JA, Perlmutter JS, Hershey T. Motor asymmetry and substantia nigra volume are related to spatial delayed response performance in Parkinson disease. Brain and Cognition 2008 67: 1-10.
Hershey T, Wu J, Perantie D, Weaver P, Karimi M, Tabbal S, Perlmutter JS. Unilateral vs. bilateral STN DBS effects on working memory and motor function in Parkinson disease. Exp Neurology 2008 210(2): 402-8.
Perantie D, Wu J, Lim A, Warren S, Koller J, Black KJ, Hershey T. Brain volume differences associated with severe hypoglycemia and chronic hyperglycemia in children with T1DM. Diabetes Care 2007 30(9): 2331-2337.
Last Updated: 08/27/2009 |