Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
Volume 1862, Issue 5, Pages 915-925Publisher
ELSEVIER
DOI: 10.1016/j.bbadis.2016.01.015
Keywords
Alzheimer's disease; Cognitive impairment; Dementia; Microinfarcts; Neuroimaging; Post-stroke dementia; Stroke; White matter; Vascular dementia
Funding
- Medical Research Council (UK)
- Alzheimer's Research UK
- Dunhill Medical Trust (UK)
- Newcastle National Institute for Health Research Biomedical Research Centre in Ageing and Age Related Diseases, Newcastle upon Tyne Hospitals, NHS Foundation Trust
- MRC [G0900652, G0502157, G0500247, MR/L016451/1, G1100540, G0400074] Funding Source: UKRI
- Alzheimers Research UK [ARUK-PG2013-22] Funding Source: researchfish
- Medical Research Council [G0502157, G0500247, G1100540, MR/L016451/1, G0400074, G0900652] Funding Source: researchfish
- The Dunhill Medical Trust [R277/0213] Funding Source: researchfish
- Grants-in-Aid for Scientific Research [15H04271] Funding Source: KAKEN
Ask authors/readers for more resources
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. (c) 2016 The Authors. Published by Elsevier B.V.
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