期刊
ARCHIVES OF NEUROLOGY
卷 63, 期 2, 页码 189-193出版社
AMER MEDICAL ASSOC
DOI: 10.1001/archneur.63.2.189
关键词
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资金
- NIA NIH HHS [AG21491] Funding Source: Medline
- NIEHS NIH HHS [ES10126] Funding Source: Medline
Objective: To understand the relationship of apolipoprotein E (APOE) polymorphism to dementia in Parkinson disease (PD) because the APOE epsilon 4 allele is linked to Alzheimer disease. Data Source: We reviewed MEDLINE, BIOSIS Previews, and ISI Web of Science from January 1, 1966, to May 7, 2004, supplemented by citation analysis from retrieved articles. Study Selection: Case-control studies using clinical or pathologic criteria for PD and dementia, and with complete APOE genotype frequencies data. Data Extraction: We compared estimated prevalence odds ratios for dementia in PD in relation to each allele. We also looked for evidence of heterogeneity and publication bias and performed a stratified analysis on several study characteristics. Data Synthesis: Data analyses suggest publication bias and heterogeneity of source data for the epsilon 4 allele (homogeneity P = .2; Begg and Mazumdar, P = .06; and Egger et al, P =. 1). The estimated odds ratios for development of dementia in PD are 1.6 for epsilon 4 (95% confidence interval, 1.0-2.5); 1.3 for epsilon 2 (95% confidence interval, 0.73-2.4); and 0.54 for epsilon 3 (95% confidence interval, 0.18-1.6). The odds ratio estimates for epsilon 4 were higher for studies published in 1996 or later (2.3 vs 1.0) and for studies conducted outside North American sites (2.4 vs 1. 2). Conclusions: The APOE epsilon 4 allele appears to be associated with a higher prevalence of dementia in PD. Publication bias and heterogeneous source data may, however, confound this conclusion. Confirmatory studies that use standardized and validated diagnostic criteria for dementia in PD are needed.
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