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Case‐control study of the α‐synuclein interacting protein gene and Parkinson's disease
Author(s) -
Maraganore Demetrius M.,
Farrer Matthew J.,
Lesnick Timothy G.,
De Andrade Mariza,
Bower James H.,
Hernandez Dena,
Hardy John A.,
Rocca Walter A.
Publication year - 2003
Publication title -
movement disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.352
H-Index - 198
eISSN - 1531-8257
pISSN - 0885-3185
DOI - 10.1002/mds.10547
Subject(s) - genetics , linkage disequilibrium , haplotype , exon , biology , gene , synuclein , parkinson's disease , intron , parkin , alpha synuclein , restriction fragment length polymorphism , genotype , disease , medicine
We conducted a case‐control study of the α‐synuclein–interacting protein gene ( SNCAIP , also known as synphilin‐1) and Parkinson's disease (PD). A total of 319 PD cases and 195 controls were genotyped for four SNCAIP variants, including a microsatellite repeat in intron 4 and three restriction fragment length polymorphisms (RFLP) proximal to the 5′ terminal of exons 1, 4, and 6. None of the variants were found associated with PD overall. Global score statistics were not significant for four, three, and two loci haplotypes. All four loci were in linkage disequilibrium for cases, controls, or both groups combined ( P < 0.0001). Recursive partitioning showed no interactions between variants of the SNCAIP gene and variants of the α‐synuclein gene ( SNCA ) or the parkin ( PARK2 ) gene. © 2003 Movement Disorder Society