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The cause of most neurodegenerative diseases remains enigmatic. There is, however, increasing evidence implicating mitochondrial dysfunction in the pathogenesis of these disorders, as well as in normal aging. Mitochondria are unique organelles in that they contain their own DNA of 16,569 base pairs that encode cytochrome b of complex III, seven of the more than 50 protein subunits of complex I, three of 13 protein subunits of complex IV(cytochrome oxidase), and two of 12 subunits of adenosine triphosphate synthase. Nuclear DNA encodes the vast majority of mitochondrial proteins including numerous components of the electron transport chain; proteins involved in mitochondrial DNA (mtDNA) replication, transcription, and translation; and all matrix and inner and outer mitochondrial proteins, which are transported to specific mitochondrial compartments by means of signal peptides. It is therefore possible for both nuclear and mtDNA mutations to produce disruption of the electron transport chain, and there is precedent for both.
In Parkinson's disease (PD) there is strong evidence for reduced mitochondrial complex I activity both in the substantia nigra as well as in peripheral tissues, including platelets (reviewed in Beal …
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