Table 1.

Genes commonly implicated in the onset of Parkinson’s disease.

Gene	Mechanism of Action	Dominant/Recessive	Ref.
LRRK2	Mutations in PD alter kinase and GTPase activities and promote substrate phosphorylation and autophosphorylation. The link to neuronal damage is still unclear.	Late-onset autosomal dominant familial PD	[28]
PARK7	Contains the DJ-1 gene, which undergoes mutation, resulting in loss of gene expression. The mechanism of action is not elucidated, but mouse models show that the DJ-1 gene may act as a neuroprotective redox sensor.	Autosomal recessive familial PD	[29]
PINK1	Has a regulatory role in the mitochondria, with damaged mitochondria undergoing mitophagy. Mitochondrial depolarization activates PINK1 and causes phosphorylation of ubiquitin at Serine65 (Ser65). High-affinity binding to the E3 ligase ubiquitin (Parkin) primes it for phosphorylation by hPINK1 at an identical Ser65 residue residing in the N-terminal ubiquitin-like domain. The E3 ligase activity is stimulated, resulting in substrates at the outer mitochondrial membrane undergoing ubiquitylation. Direct neuronal damage is still unclear.	Early onset recessive familial PD	[30]
PRKN	Encodes RBR E3 ubiquitin–protein ligases. Mutation results in the loss of this activity, leading to protein accumulation, mitophagy, and mitochondrial dysfunction. PRKN gene is named due to the “stereotypical” phenotypic outcomes.	Autosomal recessive juvenile PD (AR-JP)	[31]
SNCA	Integral in many cellular pathways, including protein degradation, membrane interactions, dopamine release and transport regulation, maintenance of synaptic vesicle supply, autophagy–lysosome pathway, and mitochondrial dysfunction.	Autosomal dominant PD	[32]