Xuemei Huang1, Peter C Chen, Charles Poole. 1. Department of Neurology, University of North Carolina School of Medicine, Chapel Hill, NC 27599-7025, USA. xuemei@med.unc.edu
Abstract
BACKGROUND: The link of the apolipoprotein (APOE) -epsilon4 allele to Alzheimer disease (AD) has led to studies investigating the role of apoE polymorphisms in Parkinson disease (PD). The authors hypothesized that any association between PD and APOE alleles and genotypes would be too small to be detected or precisely estimated by an individual case-controlled study. METHOD: The hypothesis was tested by systematic review and meta-analysis of results from case-control studies that provided clear clinical or pathologic criteria for PD and that reported APOE genotype frequencies. Published reports were obtained from MEDLINE, Biosis Previews, and ISI Web of Science searches, supplemented by citation analysis from retrieved articles. The authors estimated and compared prevalence odds ratios (OR) for PD in relation to each allele and genotype. RESULTS: Twenty-two eligible studies were identified. There was no evidence of heterogeneity (p > 0.4) or publication bias (p > 0.2) for any allele or genotype. The estimated summary OR for one or more copies of each APOE allele was 1.20 for APOE-epsilon2 (95% CI, 1.02 to 1.42), 0.83 for APOE-epsilon3 (95% CI, 0.63 to 1.09), and 0.99 for APOE-epsilon4 (95% CI, 0.87 to 1.14). CONCLUSIONS: Unlike Alzheimer disease, for which the APOE-epsilon4 allele increases the prevalence and the APOE-epsilon2 allele is protective, the authors' analysis shows the APOE-epsilon2 allele, but not the APOE-epsilon4 allele, to be positively associated with sporadic Parkinson disease.
BACKGROUND: The link of the apolipoprotein (APOE) -epsilon4 allele to Alzheimer disease (AD) has led to studies investigating the role of apoE polymorphisms in Parkinson disease (PD). The authors hypothesized that any association between PD and APOE alleles and genotypes would be too small to be detected or precisely estimated by an individual case-controlled study. METHOD: The hypothesis was tested by systematic review and meta-analysis of results from case-control studies that provided clear clinical or pathologic criteria for PD and that reported APOE genotype frequencies. Published reports were obtained from MEDLINE, Biosis Previews, and ISI Web of Science searches, supplemented by citation analysis from retrieved articles. The authors estimated and compared prevalence odds ratios (OR) for PD in relation to each allele and genotype. RESULTS: Twenty-two eligible studies were identified. There was no evidence of heterogeneity (p > 0.4) or publication bias (p > 0.2) for any allele or genotype. The estimated summary OR for one or more copies of each APOE allele was 1.20 for APOE-epsilon2 (95% CI, 1.02 to 1.42), 0.83 for APOE-epsilon3 (95% CI, 0.63 to 1.09), and 0.99 for APOE-epsilon4 (95% CI, 0.87 to 1.14). CONCLUSIONS: Unlike Alzheimer disease, for which the APOE-epsilon4 allele increases the prevalence and the APOE-epsilon2 allele is protective, the authors' analysis shows the APOE-epsilon2 allele, but not the APOE-epsilon4 allele, to be positively associated with sporadic Parkinson disease.
Authors: Colin C McCulloch; Denise M Kay; Stewart A Factor; Ali Samii; John G Nutt; Donald S Higgins; Alida Griffith; John W Roberts; Berta C Leis; Jennifer S Montimurro; Cyrus P Zabetian; Haydeh Payami Journal: Hum Genet Date: 2008-01-22 Impact factor: 4.132
Authors: Xuemei Huang; Honglei Chen; William C Miller; Richard B Mailman; Jennifer L Woodard; Peter C Chen; Dong Xiang; Richard W Murrow; Yi-Zhe Wang; Charles Poole Journal: Mov Disord Date: 2007-02-15 Impact factor: 10.338