Date of Graduation

Fall 2014

Degree

Master of Science in Cell and Molecular Biology

Department

Biomedical Sciences

Committee Chair

Benjamin Timson

Abstract

Alzheimer's disease is a progressive, fatal neurodegenerative disease that is characterized by amyloid beta (Aβ) plaque and tau tangle deposition in the brain. The widely held amyloid cascade hypothesis suggests that Aβ plaque formation is the primary pathogenic component of Alzheimer's disease. Increased Aβ concentration results in increased formation of toxic Aβ aggregates. Human epidemiological studies have found that exercise is correlated with reduced risk for Alzheimer's disease, and some studies in transgenic mouse models of Alzheimer's disease suggest physical activity reduces soluble and insoluble Aβ levels in the brain. Other studies have found less conclusive results. I propose that this disparity may be due to sub-training exercise treatments. This study examined the effects of a 3-month exercise training regimen on Aβ levels in 6-month-old Tg2576 mice. Mice were divided into three exercise training intensity groups: high, moderate, and sedentary. Soluble Aβ and Aβ -clearance-associated protein concentrations were measured. The results demonstrate reduced Aβ levels realized in a dose-dependent manner. They also show dose-dependent increases in concentration for several clearance-associated proteins, suggesting the effects of exercise training on Aβ reduction are mediated through increased Aβ clearance from the brain.

Keywords

Alzheimer's disease, exercise, Aβ, plaque, Tg2576 mice

Subject Categories

Medical Molecular Biology

Copyright

© Kaitlin Maureen Moore

Campus Only

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