Mitochondrial damages and Parkinson's disease.
Mitochondrial damages and Parkinson's disease.
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Original abstract
The mitochondrion is an organelle that regulates a variety of cellular events, including ATP production, lipid and iron metabolism, cellular Ca(2+) concentration buffering and apoptotic and necrotic signaling. Characterization of neurotoxins that recapitulate parkinsonian phenotypes has suggested that putative environmental factors that endanger mitochondrial activity could be risk factors for Parkinson's disease. Recent advances in the genetic analyses of familial PD cases have provided molecular evidence that a subset of causative and susceptible genes of Parkinson' s disease controls mitochondrial functions. PINKI, Parkin, and Fbxo7 are suggested to be involved in mitochondrial quality control. DJ-1 protects cells from oxidative stress caused by oxidative phosphorylation (OXPHOS) in mitochondria, and CHCHD2 could regulate OXPHOS complexes. PLA2G6 is suggested to regulate phospholipid oxidation and Ca2+ dynamics. These findings contribute to the evidence that midbrain dopamiiergic neurons are particularly sensitive to mitochondrial malfunction. Further research in this area will lead to the identification of new molecular targets for Parkinson's disease therapeutics.