Authors: Ana Navarro Alberto Boveris
Publish Date: 2009/11/14
Volume: 41, Issue: 6, Pages: 517-521
Abstract
Complex factors contribute to the appearance of Parkinson’s disease PD but with a constant mitochondrial involvement There are two interdependent conditions in PD brain mitochondrial dysfunction and brain mitochondrial oxidative damage Mitochondrial dysfunction and reduced complex I activity are recognized in substantia nigra and in frontal cortex in PD patients The molecular mechanism involved in the inactivation of complex I is likely accounted by the sum of ONOO− mediated reactions reactions with free radical intermediates of the lipid peroxidation process and aminealdehyde adduction reactions The inhibitory effects on complex I lead synergistically to denaturation of the protein structure and to further increases of O 2 − and ONOO− production at the vicinity of complex I An adaptive response in PD patients has been described with increases in mtNOS activity mitochondrial mass and mitochondrial biogenesis Mitochondrial dysfunction in the human frontal cortex is to be considered a factor contributing to impaired cognition in PD
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