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Biochim Biophys Acta. 2016 May;1862(5):915-25. doi: 10.1016/j.bbadis.2016.01.015. Epub 2016 Jan 22.

Stroke injury, cognitive impairment and vascular dementia.

Author information

1
Institute of Neuroscience, Newcastle University, Campus for Ageing & Vitality, Newcastle upon Tyne, NE4 5PL, United Kingdom; Neuroscience and Ageing Research Unit, Institute for Advanced Medical Research and Training, College of Medicine, University of Ibadan, Nigeria; Department of Stroke and Cerebrovascular Diseases, National Cerebral and Cardiovascular Center, 5-7-1 Fujishiro-dai, Suita, Osaka 565-8565, Japan. Electronic address: r.n.kalaria@ncl.ac.uk.
2
Institute of Neuroscience, Newcastle University, Campus for Ageing & Vitality, Newcastle upon Tyne, NE4 5PL, United Kingdom; Neuroscience and Ageing Research Unit, Institute for Advanced Medical Research and Training, College of Medicine, University of Ibadan, Nigeria; Department of Stroke and Cerebrovascular Diseases, National Cerebral and Cardiovascular Center, 5-7-1 Fujishiro-dai, Suita, Osaka 565-8565, Japan.

Abstract

The global burden of ischaemic strokes is almost 4-fold greater than haemorrhagic strokes. Current evidence suggests that 25-30% of ischaemic stroke survivors develop immediate or delayed vascular cognitive impairment (VCI) or vascular dementia (VaD). Dementia after stroke injury may encompass all types of cognitive disorders. States of cognitive dysfunction before the index stroke are described under the umbrella of pre-stroke dementia, which may entail vascular changes as well as insidious neurodegenerative processes. Risk factors for cognitive impairment and dementia after stroke are multifactorial including older age, family history, genetic variants, low educational status, vascular comorbidities, prior transient ischaemic attack or recurrent stroke and depressive illness. Neuroimaging determinants of dementia after stroke comprise silent brain infarcts, white matter changes, lacunar infarcts and medial temporal lobe atrophy. Until recently, the neuropathology of dementia after stroke was poorly defined. Most of post-stroke dementia is consistent with VaD involving multiple substrates. Microinfarction, microvascular changes related to blood-brain barrier damage, focal neuronal atrophy and low burden of co-existing neurodegenerative pathology appear key substrates of dementia after stroke injury. The elucidation of mechanisms of dementia after stroke injury will enable establishment of effective strategy for symptomatic relief and prevention. Controlling vascular disease risk factors is essential to reduce the burden of cognitive dysfunction after stroke. This article is part of a Special Issue entitled: Vascular Contributions to Cognitive Impairment and Dementia edited by M. Paul Murphy, Roderick A. Corriveau and Donna M. Wilcock.

KEYWORDS:

Alzheimer's disease; Cognitive impairment; Dementia; Microinfarcts; Neuroimaging; Post-stroke dementia; Stroke; Vascular dementia; White matter

PMID:
26806700
PMCID:
PMC4827373
DOI:
10.1016/j.bbadis.2016.01.015
[Indexed for MEDLINE]
Free PMC Article

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