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Original Contribution
February 2007

Apolipoprotein E Gene Polymorphism, Total Plasma Cholesterol Level, and Parkinson Disease Dementia

Author Affiliations

Author Affiliations: Departments of Neurology, Ageing, Degenerative and Cerebrovascular Diseases (Drs Jasinska-Myga, Opala, Ochudlo, and Gorzkowska) and Microbiology (Dr Tustanowski), Medical University of Silesia, and Division of Clinical Psychology, Central University Hospital (Mrs Tyrpa), Katowice, Poland; and Department of Neurological Science, Rush University Medical Center, Chicago, Ill (Dr Goetz).

Arch Neurol. 2007;64(2):261-265. doi:10.1001/archneur.64.2.261

Background  Apolipoprotein E gene (APOE) polymorphism is an important determinant for the development of various cardiovascular and neurodegenerative disorders. There have been conflicting reports of association of APOE polymorphism with dementia in Parkinson disease (PD).

Objective  To determine the relationship between APOE polymorphisms and plasma cholesterol concentration, and PD with dementia (PDD).

Design  Four-year (1999-2002) case-control study.

Setting  Academic medical center with inpatient and outpatient movement disorders services.

Patients  Consecutive white patients of the same ethnic background with PD.

Interventions  Strict clinical, neuropsychological, and neuroimaging criteria were used to exclude dementia with Lewy bodies, Alzheimer disease, and vascular dementia. Findings were compared in 2 clinical groups, including 98 patients (47 men and 51 women; mean age, 71 years) with PDD and 100 patients (52 men and 48 women; mean age, 62 years) with PD without dementia.

Main Outcome Measures  Analysis of APOE genotypes and allelic frequency (polymerase chain reaction) and plasma cholesterol concentration (enzymatic assay) were evaluated by a clinician blinded to the clinical diagnosis, and findings were compared between the groups with PDD or PD without dementia. Multiple stepwise regression analysis and the Spearman rank correlation coefficient were used to evaluate relationships between dementia and both APOE polymorphism and cholesterol concentration. Statistical significance was set at P<.05.

Results  ε4 Allele frequencies were similar in PDD and PD without dementia (16.8% vs 19%, respectively). Cholesterol concentration, APOE genotypes, and allelic frequencies did not relate to PDD.

Conclusions  In contrast to Alzheimer disease, when PDD is carefully defined, it is clearly not associated with APOE polymorphisms or with a distinctive plasma cholesterol profile. Ongoing longitudinal follow-up with emphasis on autopsy recruitment will enable further analyses of biochemical alterations underlying PDD.