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Updated: Jul 23, 2026

Longitudinal In Vivo Imaging of the Cerebrovasculature: Relevance to CNS Diseases
Published on: December 6, 2016
Prevalence of cerebral vascular amyloid-beta deposition and stroke in an aging Australian population: a postmortem
F L Mastaglia1, M L Byrnes, R D Johnsen
1Centre for Neuromuscular and Neurological Disorders, Australian Neuromuscular Research Institute, University of Western Australia, QEII Medical Centre, Nedlands, WA 6009, Australia. flmast@cyllene.uwa.edu.au
Abstract:
Cerebral amyloid angiopathy (CAA) is a putative risk factor for lobar cerebral haemorrhage and infarction in the elderly. However, the prevalence of stroke in a population with CAA is not known. Amyloid-beta immunohistochemistry was used to assess CAA prevalence as a function of age, and the relationship between CAA and stroke in 100 individuals aged 50-91 years who died unexpectedly and had a Coroner's postmortem. Blocks were taken from several cortical areas and from areas of infarction or haemorrhage. Parenchymal Abeta was first found in the 6th decade, whereas vascular Abeta did not appear until the 7th decade. The prevalence of both vascular and parenchymal Abeta increased with age to a maximum in the 9th decade. The age at onset of vascular Abeta deposition was similar to that in an English study of CAA but a decade later than in Japanese studies. There was no association between the presence of vascular Abeta and cerebral haemorrhage or infarction. The findings indicate differences in the time-course of vascular and parenchymal Abeta deposition with age, as well as racial differences. The lack of association between vascular Abeta and cerebral haemorrhage or infarction indicates that, in the present population, CAA was usually asymptomatic.
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