Basic Biology of Aging: Why do Alzheimer’s Disease and Cardiovascular Disease have similar risk factors and protective drugs

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Speaker

Robert Shmookler Reis, PhD
University of Arkansas for Medical Sciences


Date & Time

June 16, 2016 at 2:30pm - 4:30pm

Location

Foege N-130

Calendar

Basic Biology of Aging

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Add to Calendar 06/16/2016 02:30 PM 06/16/2016 04:30 PM America/Los_Angeles Basic Biology of Aging: Why do Alzheimer’s Disease and Cardiovascular Disease have similar risk factors and protective drugs Basic Biology of Aging: Why do Alzheimer’s Disease and Cardiovascular Disease have similar risk factors and protective drugs

Robert Shmookler Reis, PhD
University of Arkansas for Medical Sciences
Why Attend? Why do Alzheimer’s Disease and Cardiovascular Disease have similar risk factors and protective drugs? Clues from the ‘aggregome’ Alzheimer’s Disease and cardiovascular disease obviously affect different organs, and yet they share some surprising similarities. Risk factors for both include ApoE ε4 (and protection by allele ε2), and inflammatory markers such as complement C3 and cytokines such as IL-1, IL-8 and IL-11. In long-term prospective studies, aspirin and other NSAIDs that protect against cardiovascular disease also confer risk reductions for several neurodegenerative diseases including Alzheimer’s. We have examined the proteomes of specific aggregates that are characteristic and diagnostic of Alzheimer’s disease, and find that aggregates of overlapping composition also accumulate in the mouse heart during normal aging and during hypertension induced by angiotensin-2. The nature of these shared proteins and their post-translational modifications suggest mechanisms for current and future therapeutics.
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Why Attend?

Why do Alzheimer’s Disease and Cardiovascular Disease have similar risk factors and protective drugs? Clues from the ‘aggregome’

Alzheimer’s Disease and cardiovascular disease obviously affect different organs, and yet they share some surprising similarities. Risk factors for both include ApoE ε4 (and protection by allele ε2), and inflammatory markers such as complement C3 and cytokines such as IL-1, IL-8 and IL-11. In long-term prospective studies, aspirin and other NSAIDs that protect against cardiovascular disease also confer risk reductions for several neurodegenerative diseases including Alzheimer’s. We have examined the proteomes of specific aggregates that are characteristic and diagnostic of Alzheimer’s disease, and find that aggregates of overlapping composition also accumulate in the mouse heart during normal aging and during hypertension induced by angiotensin-2. The nature of these shared proteins and their post-translational modifications suggest mechanisms for current and future therapeutics.