Based on the recommendation of Daly et al., 24 for CYP2D6 nomenclature, CYP2D6 is followed by an asterisk and a combination of Roman letters and arabic numerals distinct for each allele, with a number specifying the key mutation and, where appropriate, a letter specifying additional mutations. Trivial names are also given.
P450 enzymes and Parkinson's disease: The story so far†
Article first published online: 4 NOV 2004
Copyright © 1998 Movement Disorder Society
Volume 13, Issue 2, pages 212–220, March 1998
How to Cite
Riedl, A. G., Watts, P. M., Jenner, P. and David Marsden, C. (1998), P450 enzymes and Parkinson's disease: The story so far. Mov. Disord., 13: 212–220. doi: 10.1002/mds.870130204
- Issue published online: 4 NOV 2004
- Article first published online: 4 NOV 2004
- Manuscript Accepted: 14 JUL 1997
- Manuscript Revised: 3 JUL 1997
- Manuscript Received: 10 MAR 1997
- Parkinson's disease;
- Young-onset Parkinson's disease
Environmental or endogenous toxins may cause nigral cell death in Parkinson's disease (PD) as a result of genetic susceptibility conferred by altered expression of P450 enzymes. Attention over the last 10 years has focused on CYP2D6 polymorphisms and susceptibility to PD. This review summarizes reports arising from both phenotypic and genotypic studies involving CYP2D6 and PD. Phenotypic studies have failed to support a link between CYP2D6 and PD. The more powerful genetic studies initially indicated a link between CYP2D6B mutations and PD, but critical analysis of the literature and recent studies emerging from independent laboratories fail to confirm this. Mutations in CYP2D6B are also not implicated in familial PD. As yet, there is no conclusive evidence to suggest that CYP2D6 polymorphisms confer susceptibility to PD. Whether polymorphisms in other P450s (for example, CYP1A1 and CYP2E1) are implicated in PD remains to be established.