Parkinson’s disease (PD) is a common neurodegenerative disease which frequently leads to neurological disability. Medical and surgical therapies ameliorate the symptoms and cellular replacement is a potential therapeutic option. Numerous monogenic genes have been associated with familial forms of PD. However, these account for only 10% of the PD population. The vast majority of PD patients do not have a family history and the relative contribution of genes and environmental factors in these cases of sporadic PD4 still remains to be elucidated. A few common genetic risk variants have been found in association with PD but these are unlikely to explain the etiology for all the cases. In the past few years, numerous investigators have utilised the genome-wide association study (GWAS) approach to unravel risk loci for sporadic PD. As GWAS studies are not hypothesis-driven, the identification of genetic markers provide an opportunity for unbiased correlation with known existing pathological processes such as mitochondrial dysfunction, proteasomal impairment, unfolded protein, oxidative stress and abnormal protein accumulation. Thus far, GWASs have provided consistent associations with alpha synuclein (SNCA) and tau (MAPT). However, the most recent GWAS study by Hamza and colleagues8 has for the first time identified a genetic marker that is linked to inflammation, providing a different perspective to the underlying pathophysiologic mechanism of PD.
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