期刊
JOURNAL OF THE NEUROLOGICAL SCIENCES
卷 322, 期 1-2, 页码 141-147出版社
ELSEVIER
DOI: 10.1016/j.jns.2012.07.032
关键词
Ageing; Alzheimer's disease; Dementia; Diabetes; Diet; Hypertension; Physical activity; Stroke; Vascular dementia; White matter lesions
资金
- Medical Research Council (UK) [G0500247, G0700718]
- CADASIL Trust (UK)
- US National Institutes of Health (NINDS) grant [NS054047]
- Alzheimer's Research Trust (UK)
- International Brain Research Organisation (IBRO) Research Fellowship
- MRC [G0500247, G0700718, G0900652, G0502157, G0400074, G1100540] Funding Source: UKRI
- Grants-in-Aid for Scientific Research [23390233] Funding Source: KAKEN
- Medical Research Council [G0900652, G0502157, G0400074, G0500247, G0700718, G1100540] Funding Source: researchfish
In recent years there has been increased interest in whether vascular disease contributes to Alzheimer's disease (AD). This review considers how modifiable risk factors such as hypertension, atherosclerosis, diabetes, dyslipidaemia and adiposity may impact on vascular structure and function to promote neurodegenerative processes and instigate AD. The presence of vascular pathology involving arterial stiffness, arteriolosclerosis, endothelial degeneration and blood brain barrier dysfunction leads to chronic cerebral hypoperfusion. Pathological changes in human brain and animal studies suggest cerebral hypoperfusion which in turn induces several features of AD pathology including selective brain atrophy, white matter changes and accumulation of abnormal proteins such as amyloid beta. Cerebral pathological changes may be further modified by genetic factors such as the apoliopoprotein E epsilon 4 allele. Although tau hyperphosphorylation and tangle formation still needs robust explanation further support for the notion that vascular pathology influences AD changes is provided by the evidence that interventions which improve vascular function attenuate AD pathology. (c) 2012 Elsevier B.V. All rights reserved.
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