Thesis (M. Phil.)--University of Hong Kong, 1978. / Xeorx copy of typescript.

No description available.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1958. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 81-84).

Thesis (M.Phil.)--University of Hong Kong, 1978. / Also available in print.

This document only includes an excerpt of the corresponding thesis or dissertation. To request a digital scan of the full text, please contact the Ruth Lilly Medical Library's Interlibrary Loan Department (rlmlill@iu.edu).

published_or_final_version / Pathology / Master / Master of Philosophy

Thesis (Ph.D)--Virginia Commonwealth University, 2009. / Prepared for: Dept. of Pharmaceutics. Title from title-page of electronic thesis. Bibliography: leaves 249-255.

Diss. (sammanfattning) Stockholm : Karol. inst., 2006. / Härtill 4 uppsatser.

Thesis (M.S.)--University of Nevada, Reno, 2008. / "December, 2008." Includes bibliographical references. Online version available on the World Wide Web.

Alzheimer’s disease (AD) is a widespread neurodegenerative disorder that affects tens of millions of patients worldwide. Throughout the last two decades an incredible amount of time and resources have been funneled into hopefully finding medications that would provide a cure. Unfortunately, no such compound has been identified and instead the only FDA approved medications for AD to date target symptomatic management and may not even be effective for longer than a couple of years. To this end, this paper sets out to identify modifiable risk factors for AD as well as provide recommendations for clinicians on how best to utilize the tools currently available to them to treat AD. Additionally this paper addresses common flaws in AD clinical trial study designs and provides future research directions to expand outside of the popular amyloid hypothesis and instead potentially focus on a multi-pathway mechanism of the disease. The following thesis will outline several potential mechanisms that can lead to the hallmark pathologies seen in AD, primarily amyloid deposition and neurofibrillary tangles as well as neuronal death. The majority of commercial and research interest into AD has been focused on the amyloid hypothesis and the notion that stopping the formation of amyloid plaques would stop the disease course. However, in recent years other mechanisms and neurotoxic pathways such as inhibition of tricarboxylic acid (TCA) cycle enzymes, neuroinflammation, and tauopathy have been shown to contribute both to the formation of amyloid plaques as well as contributing to AD pathology in their own right. The modifiable risk factors explored in this paper include the effects of triglycerides as well as intake of antioxidant vitamins and omega-3-fatty acids, both of which are beneficial for brain health. This paper will also highlight some of the extensive research on the Apolipoprotein E gene and the effects the various alleles have on AD risk. These being the putative protective effect of the APOE2 allele, “neutral” effect of the most commonly found APOE3 allele, and finally the deleterious effects of the APOE4 allele, believed to be the strongest genetic risk factor for late-onset AD.