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    The Metabolic Relationship between Type 2 Diabetes and Alzheimer's Disease

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    Author
    Ayala, Dilia
    Issue Date
    2019
    Keywords
    AD
    Alzheimer's Disease
    Amyloid plaques
    insulin resistance
    T2D
    Tau
    Advisor
    Zinsmaier, Konrad E.
    
    Metadata
    Show full item record
    Publisher
    The University of Arizona.
    Rights
    Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction, presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
    Abstract
    Regulation of blood glucose is responsible for maintaining a continuous supply of energy moving throughout the human body; excess glucose is toxic, while insufficient glucose can lead to impairment in insulin secretion, ketoacidosis, coma, and death1. Fluctuating continuously between fasting and post-eating modes, blood glucose homeostasis is regulated by a negative feedback system regulating as needed to preserve adequate insulin synthesis, secretion, and the body’s need for glucose-derived energy2,3. Dysregulation of the glucose-insulin feedback loop can contribute to the pathogenesis of various detrimental health disorders, including two of the most common chronic and debilitating diseases of Western Society, Alzheimer’s Disease (AD) and Type 2 Diabetes (T2D)4. While T2D is a chronic metabolic disorder, and AD is a chronic neurodegenerative disorder, there are potential pathophysiological connections between the two. Metabolic changes associated with T2D such as hyperglycemia and obesity, have been shown to induce known pathologies associated with AD such as Amyloid Beta (Aβ) plaques, neurofibrillary tangles (NFTs), and neuronal death5. Metabolic connections between AD/T2D suggest a common disease mechanism. Understanding the relationship between these two diseases could lead to new potential therapeutic treatments for AD. I hypothesize that correlation between T2D and AD shared pathologies indicates causation for the development of AD and AD-like dementia; thus, identifying additional biomarkers for early stages of AD could potentially lead to new diagnostic tests to help delay the onset of AD.
    Type
    text
    Electronic Thesis
    Degree Name
    M.S.
    Degree Level
    masters
    Degree Program
    Graduate College
    Cellular and Molecular Medicine
    Degree Grantor
    University of Arizona
    Collections
    Master's Theses

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