Parkinsons disease (PD) is the second most common neurodegenerative disorder next to Alzheimers disease. It accounts for about 0.2 to 1% of the age of 65 ? 69 and raises to 1 ? 2% of the age of 80 and above. It is mainly characterised by the involvement of the four classical symptoms - tremor, bradykinesia, postural instability and the rigidity. It may be due to the cause of the environmental toxins and also due to the genetic factors. There is high relationship for the PD with the environmental toxins. The enzyme CYP2D6 is one which acts on the chemical 1-methyl-4-phenyll, 2,3,6- tetrahydropyridine (MPTP), 1,2,3,4-tetrahydroisoquinoline (TIQ) and many other neurotoxins that cause the PD. An exciting possibility is that chemical transformation to produce PD toxin in the course of the detoxification mediated by CYP2D (cytochrome P450). The CYP2D comprises many isoenzymes which are involved in the metabolism of exogenous and endogenous toxins. The CYP2D subfamily comprise of genes which are highly specific for the debrisoquine- 4 hydroxylase activity. In this, the CYP2D6 is widely studied polymorphism. In the present study, we analyzed this CYP2D6*4 polymorphism in both the PD cases and controls using polymerase chain reaction (PCR) and Restriction Fragment Length polymorphism (RFLP). Bearers of the CYP2D6 gene variants may be classified as the extensive metabolizers (EM) and poor metabolizers (PM). PM allele carriers have lower gene activity and they are more prone to the environmental toxins. In this study we determined the CYP2D6*4 allele in both PD and control to evaluate the relation of this allele with the PD.

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