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A recent wave of new studies is providing novel clues to the potential involvement of mitochondria in PD. In particular, (i) mitochondria\u2010dependent programmed cell death pathways have been shown to be critical to PD\u2010related dopaminergic neurodegeneration, (ii) many disease\u2010causing proteins associated with familial forms of PD have been demonstrated to interact either directly or indirectly with mitochondria, (iii) aging\u2010related mitochondrial changes, such as alterations in mitochondrial DNA, are increasingly being associated with PD, and (iv) anomalies in mitochondrial dynamics and intra\u2010neuronal distribution are emerging as critical participants in the pathogenesis of PD. These new findings are revitalizing the field and reinforcing the potential role of mitochondria in the pathogenesis of PD. Whether a primary or secondary event, or part of a multi\u2010factorial pathogenic process, mitochondrial dysfunction remains at the forefront of PD research and holds the promise as a potential molecular target for the development of new therapeutic strategies for this devastating, currently incurable, disease.<\/jats:p>","DOI":"10.1111\/j.1471-4159.2008.05604.x","type":"journal-article","created":{"date-parts":[[2008,8,2]],"date-time":"2008-08-02T07:12:18Z","timestamp":1217661138000},"page":"317-328","source":"Crossref","is-referenced-by-count":114,"title":["Mitochondrial alterations in Parkinson\u2019s disease: new 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