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Professor, Psychiatry and Human BehaviorChief, Laboratory of Quantitative NeuroanatomyCPN Project Principal InvestigatorDirector, Imaging CorePhone: (601) 984-5898
Neuro-anatomy and quantitative histopathology
My research focusses on quantitative morphology of prefrontal cortex from postmortem brain tissue of individuals diagnosed with major depression and age-matched healthy controls. In particular, the relationship between alterations in the specific subpopulations of cortical glial and neuronal cells and serotonin and glutamate neurotransmitter systems in depression is examined by using immunohistochemical and molecular techniques.
Growing evidence indicates a bi-directional link between major depressive disorder and cardiovascular disease. Depression might precipitate a malfunction of the cardiovascular system, and cardiovascular disorders may precede depressive episodes. Clinical studies report impairment of endothelial functions and increased inflammatory markers (risk factor for cardiovascular disease) in depressed patients. In vivo neuroimaging studies demonstrate gross morphological pathology of blood vessels in the prefrontal cortex (PFC) in depression. However, no studies of vascular morphology and related growth factors at the microscopic and molecular level have been conducted in depression to date. Our preliminary data on microscopic analysis of vessel number and morphology in postmortem brain tissue reveal significant increases in the density of abnormal vessels in the prefrontal cortex (PFC) in depression. These vascular changes were observed in the same subjects that were used in our previous cell counting studies on reductions in the density of neurons and glial cells. Moreover, our recent gene expression studies in these depressed subjects reveal downregulation of genes for fibroblast growth factor (FGF) and brain-derived neurotrophic factor (BDNF), and rodent studies indicate that these factors are reduced in stressed animals and elevated after treatment with electroconvulsive shock or antidepressants. Thus, we hypothesize that in depression there are alterations in vascular morphology that are associated with deficits in angiogenic and neurotrophic factors as well as pathology of neurons and glial cells in the PFC. We further hypothesize that these changes are due to the depressive disorder itself and not due to treatment with antidepressant medication, therefore they will not be observed in the PFC of monkeys treated with antidepressants. The above hypothesis will be tested on sections from human postmortem PFC by:
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