Metabolic defects shared by Alzheimer?s disease and diabetes: A focus on mitochondria

被引:23
|
作者
Carvalho, Cristina [1 ,2 ,3 ]
Moreira, Paula I. [1 ,2 ,4 ]
机构
[1] Univ Coimbra, CNC Ctr Neurosci & Cell Biol, Coimbra, Portugal
[2] Univ Coimbra, CIBB Ctr Innovat Biomed & Biotechnol, Coimbra, Portugal
[3] Univ Coimbra, IIIUC Inst Interdisciplinary Res, Coimbra, Portugal
[4] Univ Coimbra, Inst Physiol, Fac Med, Coimbra, Portugal
关键词
OXIDATIVE STRESS; INSULIN-RESISTANCE; COGNITIVE DEFICIT; HIGH-GLUCOSE; BRAIN; DYSFUNCTION; DYSREGULATION; EXPRESSION; AUTOPHAGY; PEPTIDE;
D O I
10.1016/j.conb.2023.102694
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Type 2 diabetes (T2D) and Alzheimer's disease (AD) are two global epidemics that share several metabolic defects, such as insulin resistance, impaired glucose metabolism, and mito-chondrial defects. Importantly, strong evidence demonstrates that T2D significantly increases the risk of cognitive decline and dementia, particularly AD. Here, we provide an overview of the metabolic defects that characterize and link both pathol-ogies putting the focus on mitochondria. The biomarker po-tential of mitochondrial components and the therapeutic potential of some drugs that target and modulate mitochondria are also briefly discussed.
引用
收藏
页数:10
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