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The Mitochondrial Connection in Parkinson's Disease
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DOI:10.1101/cshperspect.a041891.png)
Abstract
En 中文
Mitochondria are highly dynamic organelles with complex structural features that perform several essential cellular functions, including energy production by oxidative phosphorylation, regulation of calcium and lipid homeostasis, and control of programmed cell death. Given their critical role, alterations in mitochondrial biology can lead to neuronal dysfunction and death. Defects in mitochondrial respiration, especially in oxidative energy production, have long been thought to be implicated in the etiology and pathogenesis of Parkinson's disease. However, given the multifaceted roles of mitochondria in health and diseases, the putative role of mitochondria in Parkinson's disease likely extends well beyond defective respiration. As such, mitochondrial dysfunction represents a promising target for disease-modifying therapies in Parkinson's disease and related conditions.
Keywords:
ELECTRON-TRANSPORT CHAIN
PROGRAMMED CELL-DEATH
COMPLEX-I DEFICIENCY
ALPHA-SYNUCLEIN
ENDOPLASMIC-RETICULUM
SUBSTANTIA-NIGRA
LIFE-SPAN
OXIDATIVE STRESS
DOPAMINERGIC-NEURONS
DNA DELETIONS
Journal
IF:
10.1
Papers:
3.0K
Citations:
1.3W
