Date of Award

Spring 2016

Department

Chemistry

First Advisor

Dr. Yuh-Cherng Chai

Abstract

Alzheimer’s Disease (AD) is a progressive neurodegenerative disorder that has become the sixth leading cause of death in the United States. The most notable neuropathological hallmarks of AD are the accelerated accumulation of β-amyloid deposits around neurons and the accumulation of neurofibrillary tangles (NFT) within neurons. These abnormalities block proteasome function, inhibit mitochondrial function, alter biometal levels, stimulate inflammatory processes, disrupt synaptic communication, and ultimately result in cell death. Mitochondrial dysfunction has been cited as an underlying cause of AD pathologies, specifically by enhancing the production and accumulation of β-amyloid. Once the β-amyloid oligomers form, they disrupt the Ca2+ signals of the astrocytes by forming calcium ion channels or influencing the existent calcium ion channels. The calcium disruption causes glutathione depletion, which leaves cells susceptible to further damage by oxidative stress. Oxidative stress, also enhanced by the mitochondrial dysfunction, has been extensively reported as having a major role in the development of neurodegenerative diseases. Thus, a vicious cycle ensues in which oxidative stress further enhances AD pathologies and further damages the neurons and astrocytes.

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