scholarly journals Non-replication of association for six polymorphisms from meta-analysis of genome-wide association studies of Parkinson's disease: Large-scale collaborative study

Author(s):  
Evangelos Evangelou ◽  
Demetrius M. Maraganore ◽  
Grazia Annesi ◽  
Laura Brighina ◽  
Alexis Brice ◽  
...  
2019 ◽  
Vol 18 (12) ◽  
pp. 1091-1102 ◽  
Author(s):  
Mike A Nalls ◽  
Cornelis Blauwendraat ◽  
Costanza L Vallerga ◽  
Karl Heilbron ◽  
Sara Bandres-Ciga ◽  
...  

2017 ◽  
Vol 49 (10) ◽  
pp. 1511-1516 ◽  
Author(s):  
Diana Chang ◽  
◽  
Mike A Nalls ◽  
Ingileif B Hallgrímsdóttir ◽  
Julie Hunkapiller ◽  
...  

2021 ◽  
Author(s):  
Dongbing Lai ◽  
Babak Alipanahi ◽  
Pierre Fontanillas ◽  
Tae‐Hwi Schwantes‐An ◽  
Jan Aasly ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Kuo-Hsuan Chang ◽  
Chiung-Mei Chen ◽  
Yi-Chun Chen ◽  
Hon-Chung Fung ◽  
Yih-Ru Wu

Previous genome-wide association studies in Caucasian populations suggest that genetic loci in amino acid catabolism may be associated with Parkinson’s disease (PD). However, these genetic disease associations were limitedly reported in Asian populations. Herein, we investigated the effect of top three PD-associated genetic variants related to amino acid catabolism in Caucasians listed on the top risk loci identified by meta-analysis of genome-wide association studies in PDGene database, including aminocarboxymuconate-semialdehyde decarboxylase- (ACMSD-) transmembrane protein 163 (TMEM163) rs6430538, methylcrotonyl-CoA carboxylase 1 (MCCC1) rs12637471, and branched-chain ketoacid dehydrogenase kinase- (BCKDK-) syntaxin 1B (STX1B) rs14235, by genotyping 599 Taiwanese patients with PD and 598 age-matched control subjects. PD patients demonstrate similar allelic and genotypic frequencies in all tested genetic variants. These ethnic discrepancies of genetic variants suggest a distinct genetic background of amino acid catabolism between Taiwanese and Caucasian PD patients.


2013 ◽  
Vol 34 (6) ◽  
pp. 1708.e7-1708.e13 ◽  
Author(s):  
Lasse Pihlstrøm ◽  
Gunnar Axelsson ◽  
Kari Anne Bjørnarå ◽  
Nil Dizdar ◽  
Camilla Fardell ◽  
...  

2019 ◽  
Author(s):  
Jonggeol Jeffrey Kim ◽  
Sara Bandres-Ciga ◽  
Cornelis Blauwendraat ◽  
Ziv Gan-Or ◽  

AbstractMultiple genes have been implicated in Parkinson’s disease (PD), including causal gene variants and risk variants typically identified using genome-wide association studies (GWAS). Variants in the alcohol dehydrogenase genes ADH1C and ADH1B are among the genes that have been associated with PD, suggesting that this family of genes may be important in PD. As part of the International Parkinson’s Disease Genomics Consortium’s (IPDGC) efforts to scrutinize previously reported risk factors for PD, we explored genetic variation in the alcohol dehydrogenase genes ADH1A, ADH1B, ADH1C, ADH4, ADH5, ADH6, and ADH7 using imputed GWAS data from 15,097 cases and 17,337 healthy controls. Rare-variant association tests and single-variant score tests did not show any statistically significant association of alcohol dehydrogenase genetic variation with the risk for PD.


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