Parkinson’s disease (PD) is a neurodegenerative disorder that progressively deteriorates the nervous system. Its causes are multifaceted, involving environmental influences, genetic predispositions, and epigenetic modifications. The main and inciting symptoms of PD are a combination of motor (bradykinesia, rest tremor and rigidity) and non-motor (hallucinations, compulsive behaviours and sleep disorders) symptoms. The existing treatments are mainly composed of a combination of medications that focus on treating the symptoms of the disease by replacing the lost dopamine without identifying the cause of the disease. Although beneficial, these therapies display a concerning amount of heterogeneity in drug response. Pharmacogenetics, a part of pharmacogenomics, helps to highlight the genetic factors that contribute to such heterogeneity in drug response. In the treatment of patients with PD, pharmacogenetic studies are particularly important given the variability of results, primarily concerning levodopa and dopaminergic therapies. This review covers the genetic mutation related to PD genes such as LRRK2, SNCA, and PARK2, which will be taken into account concerning their effects on disease progression and drug response. Genetic polymorphisms can significantly modulate the efficacy and adverse effects of drugs in patients with PD, influencing drug metabolism, transport, and receptor binding, among others, and involve genes such as CYP2D6 and COMT. This would be achieved through the application of pharmacogenetic insights that allow for tailored therapy approaches, optimize dosages, reduce adverse effects, and ensure better patient outcomes. Personalized medicine in PD could potentially enable improvement in treatment strategies based on an individual's genetic profile and thereby enhance management for this complex disease.
Pujari et al. (Wed,) studied this question.
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