Mitochondrial Perturbation in Alzheimer's Disease and Diabetes

被引:32
作者
Akhter, F. [1 ]
Chen, D. [1 ]
Yan, S. F. [1 ]
Yan, S. S. [1 ]
机构
[1] Univ Kansas, Sch Pharm, Higuchi Biosci Ctr, Lawrence, KS 66045 USA
来源
MOLECULAR BIOLOGY OF AGING | 2017年 / 146卷
关键词
A-BETA ACCUMULATION; AMYLOID PRECURSOR PROTEIN; HIPPOCAMPAL SYNAPTIC PLASTICITY; PERMEABILITY TRANSITION PORE; GAMMA-SECRETASE ACTIVITY; MOUSE MODEL; OXIDATIVE STRESS; TAU-HYPERPHOSPHORYLATION; ULTRASTRUCTURAL-CHANGES; IMPROVES MITOCHONDRIAL;
D O I
10.1016/bs.pmbts.2016.12.019
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Mitochondria are well-known cellular organelles that play a vital role in cellular bioenergetics, heme biosynthesis, thermogenesis, calcium homeostasis, lipid catabolism, and other metabolic activities. Given the extensive role of mitochondria in cell function, mitochondrial dysfunction plays a part in many diseases, including diabetes and Alzheimer's disease (AD). In most cases, there is overwhelming evidence that impaired mitochondrial function is a causative factor in these diseases. Studying mitochondrial function in diseased cells vs healthy cells may reveal the modified mechanisms and molecular components involved in specific disease states. In this chapter, we provide a concise overview of the major recent findings on mitochondrial abnormalities and their link to synaptic dysfunction relevant to neurodegeneration and cognitive decline in AD and diabetes. Our increased understanding of the role of mitochondrial perturbation indicates that the development of specific small molecules targeting aberrant mitochondrial function could provide therapeutic benefits for the brain in combating aging-related dementia and neurodegenerative diseases by powering up brain energy and improving synaptic function and transmission.
引用
收藏
页码:341 / 361
页数:21
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