title: Apolipoprotein E gene polymorphism, total plasma cholesterol level, and Parkinson disease dementia.
abstract: 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.
authors.affiliation: Department of Neurology, Ageing, Degenerative and Cerebrovascular Diseases, Medical University of Silesia, Central University Hospital, Medykow 14, Katowice 40-752, Poland. bmyga@wp.pl
authors.forename: Barbara
authors.initials: B
authors.lastname: Jasinska-Myga
authors.forename: Grzegorz
authors.initials: G
authors.lastname: Opala
authors.forename: Christopher G
authors.initials: CG
authors.lastname: Goetz
authors.forename: Jerzy
authors.initials: J
authors.lastname: Tustanowski
authors.forename: Stanislaw
authors.initials: S
authors.lastname: Ochudlo
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Gorzkowska
authors.forename: Jadwiga
authors.initials: J
authors.lastname: Tyrpa
mesh_terms: 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
chemical_list: D053327:Apolipoprotein E4