As the second most prevalent neurodegenerative disease worldwide (Dorsey et al., 2018), Parkinson disease (PD) is a debilitating, progressive motor disorder characterised by degeneration of the nigrostriatal dopaminergic pathway. A hypokinetic movement disorder, its symptomology arises from the loss of dopaminergic innervation of motor nuclei in the basal ganglia which results in the characteristic tetrad of motor symptoms; bradykinesia (slowness of movement), rigidity, postural instability and resting tremor. Parkinson's patients may also present with non-motor symptoms, some of which arise in the prodromal phase before onset of motor abnormalities.These early symptomatic changes may include olfactory dysfunction, depression, sleep disturbances, gastrointestinal changes and pain (Schrag et al., 2019). Recent estimates suggest that PD affects approximately ten million individuals worldwide (Dorsey et al., 2007;Marras et al., 2018). The underlying aetiology of PD is multifactorial, with complex interplay of genetic and environmental risk factors converging to confer increased disease risk.The first genetic risk factor discovered for PD was the SNCA gene (Polymeropoulos et al., 1997). Since its discovery, SNCA and the α-synuclein (α-syn) protein which it encodes have been extensively researched, with over 12,000 research papers published (as of 24th September 2020). α-syn is a major protein constituent of Lewy bodies, distinctive intracellular protein aggregates which are found in the surviving nigrostriatal dopaminergic neurons of PD patient
Parkinson’s disease (PD) is a devastating neurological movement disorder. Since its first discovery 200 years ago, genetic and environmental factors have been identified to play a role in PD development and progression. Although genetic studies have been the predominant driving force in PD research over the last few decades, currently only a small fraction of PD cases can be directly linked to monogenic mutations. The remaining cases have been attributed to other risk associated genes, environmental exposures and gene–environment interactions, making PD a multifactorial disorder with a complex etiology. However, enormous efforts from global research have yielded significant insights into pathogenic mechanisms and potential therapeutic targets for PD. This review will highlight mitochondrial dysfunction as a common pathway involved in both genetic mutations and environmental toxicants linked to PD.
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