Debrisoquine hydroxylase gene polymorphism in familial Parkinson's disease.

The CYP2D6B allele is not overrepresented in a population of German patients with idiopathic Parkinson's disease.

The frequency of the CYP2D6B allele of the gene for debrisoquine 4-hydroxylase was studied in 115 patients with sporadic idiopathic Parkinson's disease, 55 of their healthy siblings, 63 patients with familial Parkinson's disease, 55 unaffected relatives, and 92 patients with Alzheimer's disease and 73 age matched healthy controls. By contrast with several previous studies, no significant variat...

NcoI RFLP in the pseudogene (CYP2D8P) of the human debrisoquine 4-hydroxylase locus.

Astrocytic Brain Tumors and Isolated Demyelinating Lesions of the Type Seen

8. Golbe L1, Di Iorio G, Sanges G, et al. Clinical genetic analysis of Parkinson’s disease in the contursi kindred. Ann Neurol 1996;40:767-775 9. Smith CAD, Gough AC, Leigh I ”, et al. Association between the CYP2D6-debrisoquine hydroxylase polymorphism and susceptibility to Parkinson’s disease. Lancet 1992;339: 1375-1377 10. Gasser T, Wszolek ZK, Troffater J, et al. Genetic linkage studies in ...

Characterization of a human liver cytochrome P-450 involved in the oxidation of debrisoquine and other drugs by using antibodies raised to the analogous rat enzyme.

Debrisoquine 4-hydroxylase activity is a prototype for genetic polymorphism in oxidative drug metabolism in humans; approximately 10% of Caucasian populations exhibit the poor metabolizer phenotype, and the clearance of at least 14 other drugs has been shown to be deficient in patients exhibiting this phenotype. Antibodies prepared to a cytochrome P-450 shown to be responsible for debrisoquine ...

Polymorphisms of the CYP2D6 gene increase susceptibility to ankylosing spondylitis.

Ankylosing spondylitis (AS) is a common and highly familial rheumatic disorder. The sibling recurrence risk ratio for the disease is 63 and heritability assessed in twins >90%. Although MHC genes, including HLA-B27, contribute only 20-50% of the genetic risk for the disease, no non-MHC gene has yet been convincingly demonstrated to influence either susceptibility to the disease or its phenotypi...