期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 85, 期 3, 页码 943-955出版社
IOS PRESS
DOI: 10.3233/JAD-215231
关键词
Alzheimer's disease; cognitive impairment; dementia; hypertension; inflammation; neuroinflammation; reninangiotensin system; vascular dementia
资金
- National Foundation for Medical Research Innovation
- National Institute on Aging/National Institute of Health [5 R03 AG05495002]
Hypertension is a major risk factor for vascular dementia and Alzheimer's disease, and chronic activation of the renin-angiotensin system contributes to neuroinflammation. Neuroinflammation induced by chronic RAS activation plays a key role in the pathogenesis of dementia, leading to cognitive impairment.
Hypertension is a major risk factor for the pathogenesis of vascular dementia and Alzheimer's disease. Chronic activation of the renin-angiotensin system (RAS) contributes substantially to neuroinflammation. We propose that neuroinflammation arising from chronic RAS activation can initiate and potentiate the onset of hypertension and related dementia. Neuroinflammation induced by chronic activation of the RAS plays a key role in the pathogenesis of dementia. Increased levels of pro-inflammatory cytokines tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, and transforming growth factor (TGF)-beta have been reported in brain tissue of vascular dementia patients and animal models of vascular dementia induced by either angiotensin II infusion or transverse aortic coarctation. It is proposed that neuronal cell death and synaptic dysfunction induced by neuroinflammation lead to cognitive impairment in dementia. The neuroprotective RAS pathway, regulated by angiotensin-converting enzyme 2 (ACE2) which converts angiotensin II into angiotensin-(1-7), can attenuate hypertension and dementia. Furthermore, the use of anti-hypertensive medications in preventing dementia or cognitive decline in hypertensive patients and animal models of dementia have mostly been beneficial. Current evidence suggests a strong link between RAS induced neuroinflammation and the onset of hypertension and dementia, which warrants further investigation. Strategies to counteract an overactive RAS and enhance the neuroprotective arm of the RAS may help prevent or improve cognitive impairment associated with hypertension.
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