Aetiopathogenesis of Parkinson’s disease

Abstract

Parkinson’s disease (PD) is characterised both clinically and pathologically by features that distinguish it from other parkinsonian disorders including, for instance, multiple system atrophy and progressive supranuclear palsy. The aetiologies of PD includes both genetic and environmental influences. Several single gene causes of autosomal dominant and recessive PD have been described. Recent genome-wide association (GWA) studies have identified a number of risk alleles for PD. No specific environmental cause has been defined but several factors have been described which influence the risk for PD. Mitochondrial dysfunction, free radical mediated damage, inflammatory change and proteasomal dysfunction have been thought to play a role in PD pathogenesis. Autophagy is now recognised as an important component of the cell’s mechanism for protein turnover and has relevance for PD. There is some convergence and overlap of pathogenetic pathways between environmental and genetic factors. The importance of identifying the molecular and biochemical events that lead to PD lies in the prospect that novel drug targets will emerge and that new compounds will be developed that slow the progression of the disease.