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Association analysis of the genotype data was conducted with PLINK (Purcell et al., 2007). Cochran-Armitage (Armitage, 1955) trend tests were calculated at each SNP to assess allelic association. Additional analyses evaluating dominant, recessive and genotypic exposures were performed using logistic regression in PLINK. To avoid over-correcting for multiple comparisons by using the conservative http://www.selleck.cn/products/MK-1775.html Bonferroni correction, we used PLINK to generate empirically adjusted p-values based on 10,000 permutations to adjust for multiple tests (Purcell et al., 2007). Additional logistic regression analysis fitting covariates for age of onset/age at exam, sex or history of smoking was conducted to assess confounding by these variables at all SNPs. If there was an indication that an individual had reported any history of smoking, they were scored as a smoker, a non-smoker if they reported not smoking, and missing otherwise. The population proportional attributable risk (PAR%) was calculated using the formula for retrospective studies, [(SNP allele frequency)��(OR-1)]/[1+(SNP allele frequency)��(OR-1)], using the SNP allele frequency in controls as the exposure frequency, and the odds ratio (OR) in place of the relative risk (Woodward, 2005). Assessment of associated SNPs and the presence of chromosome 17q21.31 alleles in the H1-H2 haplotype clades in MAPT was accomplished using rs1981997 as a haplotype tag SNP, because the major (G) and minor (A) alleles of this SNP are fixed http://www.selleckchem.com/products/Adriamycin.html in the H1 http://www.selleckchem.com/PD-1-PD-L1.html and H2 clades respectively (Stefansson et al., 2005). A 2-locus haplotype association analysis was performed using PLINK with SNPs in the MAPT region to determine which alleles were on the H1 haplotype, which has previously been associated with PD Golbe et al., 2001; Maraganore et al., 2001; Martin et al., 2001; Farrer et al., 2002; Skipper et al., 2004; Zabetian et al., 2007; Refenes et al., 2009). In addition to the statistical analysis of the joint sample, as a final check against cryptic bias arising due to genotyping error rate heterogenetity across studies, we evaluated association with meta-analysis techniques using METAL (Abecasis & Willer, 2007). In the HIHG sample no SNPs were statistically significantly associated with PD at the genome-wide level using permutation tests with a multiple testing corrected threshold of p