Apolipoprotein E gene polymorphism, total plasma cholesterol level, and Parkinson disease dementia.
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).


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


METHODS
Academic medical center with inpatient and outpatient movement disorders services. Patients Consecutive white patients of the same ethnic background with PD.


METHODS
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.


METHODS
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
Epsilon4 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.
Jasinska-Myga
Barbara
B
Department of Neurology, Ageing, Degenerative and Cerebrovascular Diseases, Medical University of Silesia, Central University Hospital, Medykow 14, Katowice 40-752, Poland. bmyga@wp.pl
Opala
Grzegorz
G
Goetz
Christopher G
CG
Tustanowski
Jerzy
J
Ochudlo
Stanislaw
S
Gorzkowska
Agnieszka
A
Tyrpa
Jadwiga
J
D000368:Aged; D000369:Aged, 80 and over; D053327:Apolipoprotein E4 / Q000235:genetics*; D016022:Case-Control Studies; D003704:Dementia / Q000150:complications / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D010300:Parkinson Disease / Q000150:complications / Q000235:genetics*; D011110:Polymorphism, Genetic; D012189:Retrospective Studies
D053327:Apolipoprotein E4