Role of Presenilin in Mitochondrial Oxidative Stress and Neurodegeneration in Caenorhabditis elegans

被引：25

作者：

Sarasija, Shaarika ^{[1
]}

Norman, Kenneth R. ^{[1
]}

机构：

[1] Albany Med Coll, Dept Regenerat & Canc Cell Biol, Albany, NY 12208 USA

来源：

ANTIOXIDANTS | 2018年 / 7卷 / 09期

基金：

美国国家卫生研究院;

关键词：

mitochondria; calcium; C; elegans; neurodegeneration; alzheimer's disease; ROS; presenilin; FAMILIAL ALZHEIMERS-DISEASE; AMYLOID PRECURSOR PROTEIN; GAMMA-SECRETASE COMPLEX; CALCIUM UNIPORTER; BETA-PROTEIN; ESSENTIAL COMPONENT; SEL-12; PRESENILIN; CORTICAL-NEURONS; LINKED MUTATIONS; NERVOUS-SYSTEM;

D O I：

10.3390/antiox7090111

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：

Neurodegenerative diseases like Alzheimer's disease (AD) are poised to become a global health crisis, and therefore understanding the mechanisms underlying the pathogenesis is critical for the development of therapeutic strategies. Mutations in genes encoding presenilin (PSEN) occur in most familial Alzheimer's disease but the role of PSEN in AD is not fully understood. In this review, the potential modes of pathogenesis of AD are discussed, focusing on calcium homeostasis and mitochondrial function. Moreover, research using Caenorhabditis elegans to explore the effects of calcium dysregulation due to presenilin mutations on mitochondrial function, oxidative stress and neurodegeneration is explored.

引用

页数：15

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