Graduate Program

Biological Sciences

Degree Name

Master of Science (MS)

Semester of Degree Completion

2006

Thesis Director

Britto Nathan

Thesis Committee Member

Gary Bulla

Thesis Committee Member

Charles Costa

Abstract

Apolipoprotein E (apoE), a prominent player in transporting cholesterol and metabolizing plasma lipoproteins, has emerged as a major risk factor in causing Alzheimer's disease (AD). ApoE, extensively expressed in the primary olfactory pathway, binds to its low-density lipoprotein receptor and related receptors to play a role both in development and in control of the immune system. Previous studies have shown that apoE is expressed at high concentrations in the olfactory nerve (ON) and around the glomeruli of the olfactory bulb (OB) and that the apoE levels in these regions increase substantially following lesioning of the olfactory epithelium (OE). Studies from our laboratory indicate that apoE plays a vital role in the ON regeneration and maturation. However the mechanism(s) underlying the contribution of apoE to neuronal functioning and developing AD are not clearly understood. In the present study, I examined the expression of apoE in the OE, effects of apoE on the neurogenesis and neuronal maturation in apoE wild-type (WT) and apoE deficient knock-out (KO) mice during embryonic and postnatal stages, and finally, the effects of apoE on neuronal regeneration in the OE following unilateral bulbectomy (OBXХ).

My results indicate that apoE is expressed in the WT mice. On the contrary, there was no apoE staining in the KO mice. My studies revealed that apoE is expressed by Sustentacular cells (Sus), Basal cells, ensheathing glial cells (EGC), endothelial cells, Bowman's gland, olfactory nerve fascicles (ONF) and the end feet of the Sus cells. This was also confirmed by double-labeling immunohistochemistry with markers to specific cell types. This suggests a role for apoE in neuronal maturation and repair.

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