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Luis V. Colom, MD, PhD VP of Research Center for Biomedical Studies Phone: 956-882-5048 Email: [email protected] Current research interest: Investigating the mechanisms underlying brain dysfunction in Alzheimer’s disease. Research: Alzheimer’s disease (AD) is the 7th leading cause of death in the United States, affecting 5.3 million people. The extracellular deposit of amyloid beta peptides (Aβ), senile plaques in cerebral cortical regions, constitutes a hallmark lesion of AD. In addition, diminished basal forebrain cholinergic and cortical glutamatergic functions observed in AD cause most of the neuropsychological deficits in AD patients. Current Studies: Aβ effects on septal neurons Limited deposition of Aβ within the hippocampus lesions axon terminals of septal cholinergic and glutamatergic neurons. Damaged hippocampal axon terminals lead to altered somatic functions and subsequent death of cholinergic and glutamatergic septal neurons (injured cortical axons will lead to neuronal death in additional basal forebrain structures). Altered properties of the surviving septal neurons Oxidative Stress Our lab focuses on septohippocampal anatomical and functional alterations in Alzheimer’s disease models. The techniques applied to this research project are mRNA extraction, Immunohistochemistry, stereology, confocal microscopy, Extracellular recordings and patch clamp recordings. Ongoing Research: Anatomical studies of septal cholinergic, GABAergic and glutamatergic neurons Theta rhythm dependent- synaptic plasticity of the hippocampus Brain processes that depend on hippocampal synaptic plasticity, such as certain learning and memory processes. Behavioral Studies: Spatial memory tests using a Barnes maze to observe alterations in Alzheimer disease models. Grant Support NIH grant SC1NS065386 to Luis V. Colom