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dc.contributor.advisorLazarov, Orly
dc.contributor.advisorMinshall, Richard D
dc.creatorBonds, Jacqueline A
dc.date.accessioned2018-11-27T16:29:31Z
dc.date.available2018-11-27T16:29:31Z
dc.date.created2018-08
dc.date.issued2018-08-23
dc.date.submittedAugust 2018
dc.identifier.urihttp://hdl.handle.net/10027/23055
dc.description.abstractType 2 Diabetes (T2D) is a risk factor for the development of late onset Alzheimer’s disease. However, this mechanism underlying induction of AD in T2D is largely unknown. Here we show that increased pro-inflammatory cytokines in diabetic mouse models db/db (Leprdb) and MKR (Ckm-IGF1RK1003R), results in depletion of the endothelial-enriched protein Caveolin-1 (Cav-1). In turn, reduced Cav-1 in the hippocampus of db/db mice causes a decrease in the expression level of insulin receptor leading to reduced, insulin transport into the brains of diabetic mice. Further, depletion of Cav-1 induces the upregulation of amyloid precursor protein (APP) and its amyloidogenic cleavage, as well as upregulation in levels of hyperphosphorylated tau. Moreover, db/db and MKR mice exhibit deficits in recognition memory and hippocampal neurogenesis. Furthermore, our results suggest that Cav-1 is essential for neural progenitor cell proliferation and maintenance in the adult brain and its depletion may compromise neurogenesis via bone morphogenetic protein (BMP) signaling. Taken together, these results suggest that loss of Cav-1 levels is a key step in the escalation of T2D into AD.
dc.format.mimetypeapplication/pdf
dc.subjectType 2 Diabetes
dc.subjectAlzheimer's disease
dc.subjectCaveolin-1
dc.subjectInflammation
dc.titleThe Role of Caveolin-1 in Type 2 Diabetes-Induced Alzheimer's Disease
dc.typeThesis
thesis.degree.departmentAnatomy and Cell Biology
thesis.degree.grantorUniversity of Illinois at Chicago
thesis.degree.levelDoctoral
thesis.degree.namePhD, Doctor of Philosophy
dc.contributor.committeeMemberLasek, Amy
dc.contributor.committeeMemberTai, Leon
dc.type.materialtext
dc.contributor.chairLarson, John R


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