title: Capillary amyloid-β protein deposition in a population-based study (Vantaa 85+).
abstract: BACKGROUND
  Capillary amyloid-β (capAβ) deposition in the cerebral cortex is the neuropathological feature providing the basis for categorizing cerebral amyloid angiopathy (CAA) into two distinct types, CAA-Type1 with capAβ and CAA-Type2 without capAβ.
  
  
  OBJECTIVE
  We investigated the neuropathological and clinical characteristics of capAβ deposition in a prospective population-based study.
  
  
  METHODS
  Vantaa 85+ includes 601 individuals aged ≥85 years, of which 300 were studied clinically and neuropathologically. 278 subjects were analyzed for the apolipoprotein E (APOE) genotype. The diagnosis of capAβ was determined using immunohistochemistry against Aβ, and of CAA using Congo red confirmed by Aβ immunohistochemistry, both analyzed in six brain areas. The severity of capAβ was graded semi-quantitatively, and the severity of CAA was based on the percentage of affected vessels. Alzheimer's disease (AD)-type neuropathology (CERAD score and Braak stage) was analyzed using standard methods.
  
  
  RESULTS
  CAA-Type1 was present in 86/300, CAA-Type2 in 135/300, and 79/300 had no CAA. CapAβ was most frequent in the occipital lobe (79/86). CAA-Type1 was associated with the severity of CAA (p <  0.001), dementia (p <  0.001), severe AD-type neuropathology (p-value 0.09 for CERAD C and 0.017 for Braak stages V-VI), and APOE ɛ4 allele carrier status (p <  0.001).
  
  
  CONCLUSIONS
  This population-based study confirmed the presence of distinct CAA-Type1 and its association with the severity of CAA, severe AD-type neuropathology, and the APOE ɛ4 carrier status. Both the severity and localization of the deposition seemed to determine the clinical significance of capAβ.
authors.affiliation: Department of Pathology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.
authors.forename: Mira
authors.initials: M
authors.lastname: Mäkelä
authors.affiliation: Department of Pathology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.
authors.forename: Anders
authors.initials: A
authors.lastname: Paetau
authors.affiliation: Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, UK.
authors.forename: Tuomo
authors.initials: T
authors.lastname: Polvikoski
authors.affiliation: Department of Pathology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.
authors.forename: Liisa
authors.initials: L
authors.lastname: Myllykangas
authors.affiliation: Department of Pathology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland.|Department of Pathology, Kanta-Häme Central Hospital, Hämeenlinna, Finland.
authors.forename: Maarit
authors.initials: M
authors.lastname: Tanskanen
mesh_terms: D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D053327:Apolipoprotein E4 / Q000235:genetics; D001344:Autopsy; D002196:Capillaries / Q000473:pathology*; D016657:Cerebral Amyloid Angiopathy / Q000473:pathology*; D005260:Female; D005387:Finland; D005838:Genotype; D006801:Humans; D007150:Immunohistochemistry; D016015:Logistic Models; D008297:Male; D015999:Multivariate Analysis; D009778:Occipital Lobe / Q000473:pathology*; D011446:Prospective Studies; D012720:Severity of Illness Index
chemical_list: D016229:Amyloid beta-Peptides; D053327:Apolipoprotein E4
keywords: Alzheimer’s disease; CAA-Type1; capillary CAA; neuropathology; population-based study