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    A Study of the Vascular Basis of Alzheimer’s Disease: The Role of Beta Amyloid (Aβ) Proteins and Saturated Fatty Acids in Endothelial Dysfunction and Inflammation

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    Author
    Buchanan, Jenna
    Affiliation
    The University of Arizona College of Medicine - Phoenix
    Issue Date
    2016-03-23
    MeSH Subjects
    Vascular Diseases
    Fatty Acids
    Amyloid
    Alzheimer Disease
    Mentor
    Migrino, Raymond Q.
    
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    Rights
    Copyright © is held by the author. Digital access to this material is made possible by the College of Medicine - Phoenix, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
    Collection Information
    This item is part of the College of Medicine - Phoenix Scholarly Projects 2016 collection. For more information, contact the Phoenix Biomedical Campus Library at pbc-library@email.arizona.edu.
    Publisher
    The University of Arizona.
    Abstract
    Background: Studies have shown that Alzheimer’s Disease (AD) is strongly associated with the presence of atherosclerosis risk factors, including hyperlipidemia (and associated increased free fatty acids), hypertension and diabetes. We tested the hypotheses that β‐ amyloid proteins (Aβ) or palmitic acid (PA), a saturated fatty acid and known atherosclerotic risk factor, cause impaired function and viability of human umbilical vein endothelial cells (HUVEC), and that together, they exert synergistic effects on HUVEC dysfunction. Methods: HUVEC were exposed for 18‐20 hours to vehicle, Aβ42 (2μM) ± PA (150μM) or PA (150μM) while some HUVEC were exposed to a 4‐hour pre‐treatment with PA (150mM) followed wash and treatment with vehicle ± Aβ42 (2μM) for 18‐20 hours. Outcomes measured included: (1) nitric oxide (NO) and measures of oxidative stress (superoxide) and nitrosative stress (peroxynitrite), (2) inflammatory and associated markers (interleukins (IL)‐6, IL‐8, Reaction for Advanced Glyocolytic End Products (RAGE) 1 and 2, and Matrix Metalloproteinases (MMP‐9) by PCR. Results: HUVECs exposed to either Aβ or PA showed impaired NO production and increased superoxide and peroxynitrite when compared to vehicle control. Co‐treatment with Aβ and PA did not cause a statistically significant change compared to Aβ or PA alone. HUVEC demonstrated variable inflammatory responses following exposure to either Aβ or PA. Treatment with PA resulted in upregulation of RAGE2 gene expression (p<0.003) and trend towards IL‐6 overexpression (p=0.059). Co‐treatment with both Aβ and PA led to an observed increase in inflammatory responses versus control, but the results did not reach statistical significance. Conclusion: Independent exposure of HUVECs to Aβ and PA caused decreased nitric oxide production and increased oxidative and nitrosative stress. HUVECs did not demonstrate Aβ‐ induced endothelial cell inflammation. Co‐treatment with 2μM Aβ and PA 150μM did not result in a synergistic or additive increase in endothelial cell inflammatory responses.
    Description
    A Thesis submitted to The University of Arizona College of Medicine - Phoenix in partial fulfillment of the requirements for the Degree of Doctor of Medicine.
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