Mitochondrial dysfunction in Parkinson's syndrome

Apart from the genetic forms of Parkinson's disease aetiology and pathogenesis of the idiopathic Parkinson's syndrome are still unsolved. While environmental noxa, genetic predisposition and advancing age are discussed as aetiologic factors, oxidative stress seems to be a central pathogenic factor. With regard to the latter, mitochondrial dysfunction plays a key role. Respiratory chain defects are systemic in Parkinson's disease. So far, no specific Parkinsonian mutations could be detected uniformly, but accumulation of somatic deletions in the mitochondrial DNA of dopaminergic neurons seems to play an important role. Additionally, oxidatively damaged complex I of the respiratory chain was detected in Parkinsonian tissue which was attributed to a potentially increased production of radicals due to mutations and/or respiratory chain inhibitors. The discovery of a close relationship between certain PARK genes and the mitochondria re-established these organelles as an important aetiopathogenic factor and has pushed them back to centre stage.