Detection of amyloid plaques in patients with post-stroke dementia.

Cognitive impairment is a common sequel to stroke; the rate of post-stroke dementia is 6% to 30%. As a predictor of long-term mortality and functional disability (independent of physical impairment), post-stroke dementia poses a huge economic and social burden in developed countries. Cerebrovascular disease may not be the only factor responsible for the cognitive decline following stroke/transient ischaemic attack. Alzheimer’s disease pathology may also play a role in poststroke dementia. Amyloid plaques are a pathological hallmark of Alzheimer’s disease. Cerebrovascular lesions and amyloid frequency co-exist with ageing. 11C-Pittsburgh Compound B (PiB) positron emission tomography (PET) can detect amyloid plaques in Alzheimer’s disease patients with high sensitivity and specificity.1 Alzheimer’s disease treatment (eg acetylcholinesterase inhibitors) may be more beneficial in patients with mixed dementia than in those with pure vascular dementia. Therefore, determining the presence of concurrent Alzheimer’s disease among patients with post-stroke dementia has clinical implications. This study aimed to determine the frequency of amyloid plaques in patients with post-stroke dementia, and whether the cognition of post-stroke dementia patients with amyloid plaques declines faster than those without.