Thesis (M.A.)--Central Connecticut State University, 2001. / Thesis advisor: C. Charles Mate-Kole. " ... in partial fulfillment of the requirements for the degree of Master of Arts in Psychology." Includes bibliographical references (leaves 36-44). Also available via the World Wide Web.

Thesis (Ph. D.)--Florida State University, 2004. / Advisor: Dr. Michelle Bourgeois, Florida State University, College of Communication, Dept. of Communication Disorders. Title and description from dissertation home page (viewed Sept. 23, 2004). Includes bibliographical references.

Thesis (Ph.D.)--Drexel University, 2010. / Includes abstract and vita. Includes bibliographical references (leaves 105-113).

Thesis (Ph. D.)--Virginia Polytechnic Institute and State University, 2005. / Includes bibliographical references (leaves 113-124). Also available online (PDF file) by a subscription to the set or by purchasing the individual file.

Thesis (Ph. D.)--Virginia Polytechnic Institute and State University, 2005. / Includes bibliographical references (leaves 113-124).

Thesis (Ph. D.)--University of North Texas, August, 2008. / Title from title page display. Includes bibliographical references.

Thesis (D. Min.)--Bethel Seminary, St. Paul, MN, 2001. / Abstract. Includes bibliographical references (leaves 159-167).

Thesis (M.S.)--University of Missouri--Columbia, 1997. / Typescript. Includes bibliographical references (leaves 34-39). Also available on the Internet.

Alzheimer's disease (AD) is characterized by neuronal atrophy caused by soluble amyloid β protein (Aβ) peptide "oligomers" and a microglial-mediated inflammatory response elicited by extensive amyloid deposition in the brain. We show that CNI-1493, a tetravalent guanylhydrazone with established antiinflammatory properties, interferes with Aβ assembly and protects neuronal cells from the toxic effect of soluble Aβ oligomers. Administration of CNI-1493 to TgCRND8 mice overexpressing human amyloid precursor protein (APP) for a treatment period of 8 wk significantly reduced Aβ deposition. CNI-1493 treatment resulted in 70% reduction of amyloid plaque area in the cortex and 87% reduction in the hippocampus of these animals. Administration of CNI-1493 significantly improved memory performance in a cognition task compared with vehicle-treated mice. In vitro analysis of CNI-1493 on APP processing in an APP-overexpressing cell line revealed a significant dose-dependent decrease of total Aβ accumulation. This study indicates that the antiinflammatory agent CNI-1493 can ameliorate the pathophysiology and cognitive defects in a murine model of AD.

This study investigated the effect of high-fat diet consumption on Alzheimer's disease-related pathology in the Tg6799 mouse model. We found that high-fat diet attenuates Alzheimer's disease-related pathology and cognitive dysfunction in Tg6799 mice and propose decreased beta-amyloid deposition due to improved autophagic-lysosomal flux as a potential, underlying mechanism.