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Genetic analysis of “leucine‐rich repeat (LRR) and immunoglobulin (Ig) domain‐containing, Nogo receptor‐interacting protein‐1 ( LINGO1 )” in two independent Chinese parkinson's disease populations
Author(s) -
Wu YihRu,
Tan EngKing,
Chen ChiungMei,
Kumar Prakash M.,
LeeChen GueyJen,
Chen SienTsong
Publication year - 2011
Publication title -
american journal of medical genetics part b: neuropsychiatric genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.393
H-Index - 126
eISSN - 1552-485X
pISSN - 1552-4841
DOI - 10.1002/ajmg.b.31124
Subject(s) - allele , leucine rich repeat , biology , genetics , parkinson's disease , genotype , phenotype , disease , dopaminergic , genetic association , gene , medicine , neuroscience , single nucleotide polymorphism , dopamine
A large genome‐wide association study has shown that the “leucine‐rich repeat (LRR) and immunoglobulin (Ig) domain‐containing, Nogo receptor‐interacting protein‐1 ( LINGO1 ) gene” is associated with an increased risk for essential tremor (ET) recently. Given the clinical phenotype overlap between Parkinson's disease (PD) and ET, and LINGO1 had also been demonstrated to play roles in the structural plasticity and integrity of the DA neurons as well as survival of dopaminergic neurons in PD animal models, it has been suggested that the LINGO1 variant could be associated with PD. Here, we report the first analysis of the LINGO1 variant rs9652490 (A > G) in two independent case–control cohorts in ethnic Chinese populations involving a total of 1,305 subjects (649 PD patients and 656 controls) from Taiwan and Singapore. We were unable to demonstrate any significant association between genotype distribution and allele frequency with risk of PD in each case–control study and in the pooled analysis. Further meta‐analysis including all published data and ours failed to demonstrate any modulatory role of rs9652490 GG genotype or G allele. LINGO1 variant rs9652490 (A > G) is unlikely to play a major role in PD in our Chinese populations. © 2010 Wiley‐Liss, Inc.