Journal
NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
Volume 64, Issue -, Pages 272-287Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neubiorev.2016.03.005
Keywords
Diabetes; Alzheimer's disease; Amyloid; Tau; Inflammation and cognition
Categories
Funding
- Larry Hillblom Foundation [2013-A-016-FEL]
- Alzheimer's Association [NIRG-15-363477]
- California Institute for Regenerative Medicine (CIRM) [TG2-01152]
- National Institutes of Health (NIH): NIH/NIA [AG027544]
- BrightFocus Foundation [A2015535S]
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Despite intensive research efforts over the past few decades, the mechanisms underlying the etiology of sporadic Alzheimer's disease (AD) remain unknown. This fact is of major concern because the number of patients affected by this medical condition is increasing exponentially and the existing treatments are only palliative in nature and offer no disease modifying affects. Interestingly, recent epidemiological studies indicate that diabetes significantly increases the risk of developing AD, suggesting that diabetes may play a causative role in the development of AD pathogenesis. Therefore, elucidating the molecular interactions between diabetes and AD is of critical significance because it might offer a novel approach to identifying mechanisms that may modulate the onset and progression of sporadic AD cases. This review highlights the involvement of several novels pathological molecular mechanisms induced by diabetes that increase AD pathogenesis. Furthermore, we discuss novel findings in animal model and clinical studies involving the use of anti-diabetic compounds as promising therapeutics for AD. (C) 2016 Elsevier Ltd. All rights reserved.
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