Brain Mitochondrial Dysfunction and Complex I Syndrome in Parkinson ́s Disease

Abstract

1.1 Clinical characteristics of Parkinson’s disease Parkinson’s disease (PD) is an old-age neurodegenerative disease with a small but significant genetic risk. The prevalence of PD is of 0.3% in the whole population, affecting more than 1% of the humans over 60 years of age (de Lau & Breteler, 2006). Parkinson s disease is characterized by the progressive loss of dopamine due to degeneration of dopaminergic neurons in the substancia nigra, striatum body and brain cortex. In addition, αsynuclein-positive Lewy bodies in brainstem and neocortex are consistently found at autopsy (Forno, 1996; Jellinger & Mizuno, 2003). Therefore, in patients with PD, movements, sleep, autonomic functions and cognition become progressively impaired. Complex factors contribute to the appearance of PD but with a constant mitochondrial involvement and a decreased capacity to produce energy (ATP) in the affected brain areas (Shapira, 1998; Shapira, 2008). Mitochondrial dysfunction in the human frontal cortex is to be considered a factor contributing to impaired cognition in PD.