Bio
We are examining the role of insulin degrading enzyme (IDE) and insulin-signaling pathways in the etiology of Alzheimer’s disease. IDE degrades both insulin and beta amyloid. Disruption of IDE could impair beta amyloid clearance, leading to its deposition into plaques. Aberrant IDE expression may also result in altered insulin levels and abnormal insulin signaling, which may play a role in the development of Alzheimer’s disease.
A second project examines mechanisms by which the hippocampus adapts to glucocorticoid exposure. Altered levels of the stress hormone cortisol have been associated with disturbances in mood, cognition and behavior. We are examining the hypothesis that chronic cortisol exposure induces a shift towards a GABAergic inhibitory phenotype as part of a compensatory adaptation to this stress hormone. Ultimately, we would like to determine if this compensatory response is impaired in individuals with glucocorticoid-associated neuropsychiatric disorders, or alternatively, if this response becomes detrimental over time.
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