Date of Award

1-1-2013

Document Type

Open Access Dissertation

Department

Biomedical Engineering

First Advisor

Melissa Moss

Abstract

In 2012 it was estimated that one in every nine Americans over the age of 65 has Alzheimer's disease (AD) (1). These patients experience gradual loss of memory, cognition, and behavioral stability eventually leading to death (2). These symptoms were first described in 1906 by Alois Alzheimer and now are the classic signs of the number one neurodegenerative disease today. Current AD therapies delay or mitigate the symptoms associated with AD to improve the quality of life for the patient; however, there is currently no cure for those that have been diagnosed. In order to develop a possible treatment for patients with mild to severe AD, the disease pathology must first be understood. One neuropathological marker for AD is the development of amyloid plaques, which are deposited around the neurons in the brain and are associated with neuronal atrophy. The main constituents of these plaques are aggregated forms of the amyloid-beta (Abeta) peptide. Thus, one possible therapeutic intervention for AD is to inhibit the formation of the Abeta aggregates.

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