title: Relation of coronary atherosclerosis and apolipoprotein E genotypes in Alzheimer patients.
abstract: OBJECTIVE
  Apolipoprotein E (apoE) epsilon 4 allele has been associated with a high risk for coronary heart disease. Increased frequency of the epsilon 4 allele has also been reported in patients with late-onset familial and sporadic Alzheimer's disease (AD). The aim of this study was to investigate the degree of coronary and cerebral atherosclerosis in a neuropathologically verified series of AD patients with different apoE genotypes. In addition, we studied the relationship between the degree of coronary and cerebral atherosclerosis and the extent of beta-amyloid (A beta) accumulation.
  
  
  METHODS
  We studied 38 subjects (32 patients with definite AD and 6 age-matched control subjects) for whom postmortem autopsy delay was less than 8 hours. ApoE genotypes were identified through Hha I digestion of the polymerase chain reaction-amplified samples. We used A beta immunohistochemistry to detect diffuse and neuritic plaques as well as cerebrovascular amyloid. The degree of coronary and cerebral atherosclerosis was rated as none, mild, moderate, or severe.
  
  
  RESULTS
  The apoE genotypes of the AD patients were epsilon 4/4 2, epsilon 3/4 19, epsilon 3/3 9, and epsilon 3/2 2. We found more severe atherosclerosis of the coronary vessels among AD patients with the apoE epsilon 4 allele compared with those AD patients without the epsilon 4 allele (chi 2 = 4.1, df = 1, P < .05). The extent of cerebral atherosclerosis did not differ among AD subgroups with and without the epsilon 4 allele. The degree of coronary or cerebral atherosclerosis was not related to the amount of amyloid accumulation in the frontal and temporal cortices or in the hippocampal structures.
  
  
  CONCLUSIONS
  This study confirms the association of apoE epsilon 4 allele with coronary atherosclerosis in AD patients.
authors.affiliation: Department of Pathology, Kuopio University Hospital, University of Kuopio, Finland.
authors.forename: O
authors.initials: O
authors.lastname: Kosunen
authors.forename: S
authors.initials: S
authors.lastname: Talasniemi
authors.forename: M
authors.initials: M
authors.lastname: Lehtovirta
authors.forename: O
authors.initials: O
authors.lastname: Heinonen
authors.forename: S
authors.initials: S
authors.lastname: Helisalmi
authors.forename: A
authors.initials: A
authors.lastname: Mannermaa
authors.forename: L
authors.initials: L
authors.lastname: Paljärvi
authors.forename: M
authors.initials: M
authors.lastname: Ryynänen
authors.forename: P J
authors.initials: PJ
authors.lastname: Riekkinen
authors.forename: H
authors.initials: H
authors.lastname: Soininen
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000483:Alleles; D000544:Alzheimer Disease / Q000209:etiology* / Q000235:genetics* / Q000401:mortality; D000682:Amyloid / Q000032:analysis; D001057:Apolipoproteins E / Q000235:genetics*; D001344:Autopsy; D001921:Brain / Q000378:metabolism / Q000473:pathology; D003324:Coronary Artery Disease / Q000150:complications* / Q000378:metabolism; D003331:Coronary Vessels / Q000378:metabolism / Q000473:pathology; D005260:Female; D005838:Genotype; D006801:Humans; D008297:Male
chemical_list: D000682:Amyloid; D001057:Apolipoproteins E