Diabetes and Alzheimer's disease crosstalk

被引:185
作者
Baglietto-Vargas, David
Shi, Jessica
Yaeger, Devin M.
Ager, Rahasson
LaFerla, Frank M.
机构
[1] Univ Calif Irvine, Dept Neurobiol & Behav, Irvine, CA 92697 USA
[2] Univ Calif Irvine, Inst Memory Impairments & Neurol Disorders, Irvine, CA 92697 USA
基金
美国国家卫生研究院;
关键词
Diabetes; Alzheimer's disease; Amyloid; Tau; Inflammation and cognition; MILD COGNITIVE IMPAIRMENT; GLYCATION END-PRODUCTS; AMYLOID-BETA-PEPTIDE; ACTIVATED PROTEIN-KINASE; BRAIN GLUCOSE-METABOLISM; GROWTH-FACTOR EXPRESSION; TRANSGENIC MOUSE MODEL; CENTRAL-NERVOUS-SYSTEM; CYTOCHROME-C-OXIDASE; WILD-TYPE TAU;
D O I
10.1016/j.neubiorev.2016.03.005
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
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.
引用
收藏
页码:272 / 287
页数:16
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