Graduation Year


Date of Submission


Document Type

Open Access Senior Thesis

Degree Name

Bachelor of Arts


W.M. Keck Science Department

Reader 1

Melissa Coleman

Reader 2

Brian Duistermars

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Alzheimer’s Disease (AD) is a degenerative neurologic disorder that is often defined by beta-amyloid (Aβ) plaques. These Aβ plaques are formed from protein pieces that are incorrectly cleaved from an amyloid precursor protein (APP). These protein segments, cleaved from APP, are toxic due to increased “stickiness”. They cling together to create protofibrils that eventually mature into neuronal plaques. Aβ plaques lead to neuronal cell death causing classic AD symptoms: memory loss, a decline in speech and motor control, and personality changes. One connection between high Aβ plaques levels and AD is chronic sleep loss or disruption. Night shift workers, even if they make up the same hours of sleep after a shift, disrupt their circadian rhythms and alter their sleep-wake cycle. Disruption of sleep leads to Aβ plaque build-up. One suggested function of REM sleep is to “flush” toxins, including these Aβ plaques. Without quality REM sleep, Aβ plaques build in the brain. By using a radiotracer, neuronal plaque level can be measured and the results compared to the varying types of night shift work. Thus, the crucial role that sleep plays in brain health may explain the underlying causes of AD.

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