Alzheimer's disease and type 2 diabetes via chronic inflammatory mechanisms

被引:55
作者
Mushtaq, Gohar [1 ]
Khan, Jalaluddin A. [1 ]
Kumosani, Taha A. [1 ,2 ]
Kamal, Mohammad A. [2 ]
机构
[1] King Abdulaziz Univ, Fac Sci, Dept Biochem, Jeddah 21589, Saudi Arabia
[2] King Abdulaziz Univ, King Fahd Med Res Ctr, Jeddah 21589, Saudi Arabia
关键词
Alzheimer's disease; Anti-inflammatory drugs; beta-Amyloid; C-reactive protein; Cytokines; Hyperinsulinemia; Inflammation; Oxidative stress; Transgenic mouse models; Tumor necrosis factor-alpha; Type 2 diabetes mellitus; BLOOD-BRAIN-BARRIER; AMYLOID-BETA PEPTIDE; C-REACTIVE PROTEIN; NF-KAPPA-B; ACTIVATED RECEPTOR-GAMMA; NECROSIS-FACTOR-ALPHA; CONVERTING ENZYME-INHIBITORS; OXIDE SYNTHASE EXPRESSION; PEROXISOME PROLIFERATOR; INSULIN-RESISTANCE;
D O I
10.1016/j.sjbs.2014.05.003
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Recent evidence has indicated that type 2 diabetes mellitus (T2DM) increases the risk of developing Alzheimer's disease (AD). Therefore, it is crucial to investigate the potential common processes that could explain this relation between AD and T2DM. In the recent decades, an abundance of evidence has emerged demonstrating that chronic inflammatory processes may be the major factors contributing to the development and progression of T2DM and AD. In this article, we have discussed the molecular underpinnings of inflammatory process that contribute to the pathogenesis of T2DM and AD and how they are linked to these two diseases. In depth understanding of the inflammatory mechanisms through which AD and T2DM are associated to each other may help the researchers to develop novel and more effective strategies to treat together AD and T2DM. Several treatment options have been identified which spurn the inflammatory processes and discourage the production of inflammatory mediators, thereby preventing or slowing down the onset of T2DM and AD. (C) 2014 Production and hosting by Elsevier B.V. on behalf of King Saud University.
引用
收藏
页码:4 / 13
页数:10
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