title: Apolipoprotein E ε2 genotype delays onset of dementia with Lewy bodies in a Norwegian cohort.
abstract: BACKGROUND
  Results conflict concerning the relevance of APOE alleles on the development of dementia with Lewy bodies (DLB), though they are well established in connection with Alzheimer's disease (AD). The role of APOE alleles in a Norwegian cohort of patients with DLB was therefore examined compared with patients with AD and healthy control individuals.
  
  
  METHODS
  The study included 156 patients with DLB diagnosed according to the consensus criteria guidelines, 519 patients diagnosed with AD according to the National Institute of Neurological and Communicative Diseases and Stroke/Alzheimer's Disease and Related Disorders Association (NINCDS/ARDRA) criteria and 643 healthy elderly volunteers. Patients were recruited through hospitals, outpatient clinics, nursing homes or from local care authorities in central and south-western parts of Norway. Healthy individuals were recruited from caregivers and societies for retired people.
  
  
  RESULTS
  Subjects carrying an APOE ε2 allele had a reduced risk for developing DLB (OR 0.4, CI 0.3 to 0.8, p=0.004), and the onset of disease was delayed by 4 years (p=0.01, Mann-Whitney U test). Conversely, the APOE ε4 allele increased the risk for development of DLB (OR 5.9, CI 2.7 to 13.0, p<0.0005 for homozygotes). Similar results were found for patients with AD regarding the effect of APOE ε2, though the protective effect appeared to be slightly less pronounced than in DLB. This study is one of the largest regarding DLB and APOE to date.
  
  
  CONCLUSIONS
  The results indicate that APOE ε2, a protective factor in AD, has a clear beneficial effect on the development of DLB also.
authors.affiliation: Faculty of Medicine, Department of Neuroscience, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
authors.forename: Guro
authors.initials: G
authors.lastname: Berge
authors.affiliation: Faculty of Medicine, Department of Neuroscience, Norwegian University of Science and Technology (NTNU), Trondheim, Norway Department of Neurology, University Hospital of Trondheim, Trondheim, Norway.
authors.forename: Sigrid B
authors.initials: SB
authors.lastname: Sando
authors.affiliation: Department of Psychiatry, Haugesund Hospital, Haugesund, Norway.
authors.forename: Arvid
authors.initials: A
authors.lastname: Rongve
authors.affiliation: Department of Neurobiology, Care Sciences, and Society, Alzheimer's Disease Research Center, Karolinska Institute, Stockholm, Sweden Department of Psychiatry, Akershus University Hospital, Norway Centre for Age-Related Medicine, Stavanger University Hospital, Stavanger, Norway.
authors.forename: Dag
authors.initials: D
authors.lastname: Aarsland
authors.affiliation: Faculty of Medicine, Department of Neuroscience, Norwegian University of Science and Technology (NTNU), Trondheim, Norway Department of Neurology, University Hospital of Trondheim, Trondheim, Norway.
authors.forename: Linda R
authors.initials: LR
authors.lastname: White
mesh_terms: D017668:Age of Onset; D000368:Aged; D000483:Alleles; D000544:Alzheimer Disease / Q000235:genetics; D053329:Apolipoprotein E2 / Q000235:genetics*; D016022:Case-Control Studies; D005260:Female; D005838:Genotype; D006801:Humans; D020961:Lewy Body Disease / Q000235:genetics*; D008297:Male; D009664:Norway / Q000453:epidemiology; D012307:Risk Factors
chemical_list: D053329:Apolipoprotein E2
keywords: Alzheimer's disease; Dementia; Genetics