期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 483, 期 4, 页码 1069-1077出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2016.07.122
关键词
Mitochondria; Calcium signaling; Endoplasmic reticulum; Mutant huntingtin; Amyloid-beta peptide; Tau
资金
- FEDER funds through Programa Operacional Factores de Competitividade COMPETE
- national funds through Fundacao para a Ciencia e a Tecnologia (FCT) by the CNC
- IBILI [UID/ NEU/04539/2013]
- FCT [SFRH/BD/86655/2012, SFRH/BPD/86551/2012]
- POPH Programa Potential Humano
- European Union
- Mantero Belard Neuroscience, SCML post-doctoral fellowship
- Mantero Belard Neuroscience prize, Santa Casa da Misericordia de Lisboa (SCML), Portugal
- Tundacao Luso-Americana para o Desenvolvimento' (FLAD) Life Science, Portugal
- Fundação para a Ciência e a Tecnologia [SFRH/BD/86655/2012] Funding Source: FCT
Mitochondria play a relevant role in Ca2+ buffering, governing energy metabolism and neuronal function. Huntington's disease (HD) and Alzheimer's disease (AD) are two neurodegenerative disorders that, although clinically distinct, share pathological features linked to selective brain damage. These include mitochondrial dysfunction, intracellular Ca2+ deregulation and mitochondrial Ca2+ handling deficits. Both diseases are associated with misfolding and aggregation of specific proteins that physically interact with mitochondria and interfere with endoplasmic reticulum (ER)/mitochondria-contact sites. Cumulating evidences indicate that impairment of mitochondrial Ca2+ homeostasis underlies the susceptibility to selective neuronal death observed in HD and AD; however data obtained with different models and experimental approaches are not always consistent. In this review, we explore the recent literature on deregulation of mitochondrial Ca2+ handling underlying the interplay between mitochondria and ER in HD and AD -associated neurodegeneration. (C) 2016 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据