The Role of Mitochondrial Calcium Homeostasis in Alzheimer's and Related Diseases

被引：67
作者：
Ryan, Kerry C. [1 ]
Ashkavand, Zahra [1 ]
Norman, Kenneth R. [1 ]
机构：
[1] Albany Med Coll, Dept Regenerat & Canc Cell Biol, Albany, NY 12208 USA
来源：
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2020年 / 21卷 / 23期
关键词：
mitochondria; calcium; neurodegeneration; Alzheimer’ s disease; MCU; ROS; presenilin; AMYLOID PRECURSOR PROTEIN; ATYPICAL RHO-GTPASES; OXIDATIVE STRESS; ENDOPLASMIC-RETICULUM; SYNAPTIC PLASTICITY; A-BETA; INTRACELLULAR CALCIUM; LIPID-PEROXIDATION; ENERGY-METABOLISM; CA2+;
D O I：
10.3390/ijms21239153
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：
Calcium signaling is essential for neuronal function, and its dysregulation has been implicated across neurodegenerative diseases, including Alzheimer's disease (AD). A close reciprocal relationship exists between calcium signaling and mitochondrial function. Growing evidence in a variety of AD models indicates that calcium dyshomeostasis drastically alters mitochondrial activity which, in turn, drives neurodegeneration. This review discusses the potential pathogenic mechanisms by which calcium impairs mitochondrial function in AD, focusing on the impact of calcium in endoplasmic reticulum (ER)-mitochondrial communication, mitochondrial transport, oxidative stress, and protein homeostasis. This review also summarizes recent data that highlight the need for exploring the mechanisms underlying calcium-mediated mitochondrial dysfunction while suggesting potential targets for modulating mitochondrial calcium levels to treat neurodegenerative diseases such as AD.
引用
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页码：1 / 17
页数：17
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