D. melanogaster, mitochondria and neurodegeneration: small model organism, big discoveries

被引:16
作者
Debattisti, Valentina [1 ]
Scorrano, Luca [1 ,2 ]
机构
[1] Venetian Inst Mol Med, Dulbecco Telethon Inst, I-35129 Padua, Italy
[2] Univ Geneva, Dept Cell Physiol & Med, CH-1206 Geneva, Switzerland
关键词
Mitochondria; Fusion-fission; Drosophila melanogaster; Dominant optic atrophy; Charcot-Marie-Tooth Ha; Neurodegenerative diseases; DYNAMIN-RELATED PROTEIN; CYTOCHROME-C RELEASE; PARKINSONS-DISEASE GENES; KINESIN HEAVY-CHAIN; ENDOPLASMIC-RETICULUM; AXONAL-TRANSPORT; OPTIC ATROPHY; HETEROZYGOUS MUTATION; CASPASE ACTIVATION; INDUCED APOPTOSIS;
D O I
10.1016/j.mcn.2012.08.007
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
In developed countries, increased life expectancy is accompanied by an increased prevalence of age-related disorders like cancer and neurodegenerative diseases. Albeit the molecular mechanisms behind the clinically, pathologically and etiologically heterogeneous forms of neurodegeneration are often unclear, impairment of mitochondrial fusion-fission and dynamics emerged in recent years as a feature of neuronal dysfunction and death, pinpointing the need for animal models to investigate the relationship between mitochondrial shape and neurodegeneration. While research on mammalian models is slowed down by the complexity of the organisms and their genomes, the long latency of the symptoms and by the difficulty to generate and analyze large cohorts, the lower metazoan Drosophila melanogaster overcomes these problems, proving to be a suitable model to study neurodegenerative diseases and mitochondria-shaping proteins. Here we will summarize our current knowledge on the link between mitochondrial shape and models of neurodegeneration in the fruitfly. This article is part of a Special Issue entitled 'Mitochondrial function and dysfunction in neurodegeneration'. (C) 2012 Published by Elsevier Inc.
引用
收藏
页码:77 / 86
页数:10
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