期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 20, 期 3, 页码 813-821出版社
IOS PRESS
DOI: 10.3233/JAD-2010-100081
关键词
Alzheimer's disease; cardiac output; cardiovascular disease; cognition
资金
- Beeson Career Development Award in Aging [K23-AG030962]
- Alzheimer's Association [IIRG-08-88733]
- Boston University Alzheimer's Disease Core Center [P30-AG013846]
- [F32-AG022773]
- NATIONAL INSTITUTE ON AGING [P30AG013846, F32AG022773, K23AG030962] Funding Source: NIH RePORTER
Heart failure has served as a clinically useful model for understanding how cardiac dysfunction is associated with neuroanatomic and neuropsychological changes in aging adults, theoretically because systemic hypoperfusion disrupts cerebral perfusion, contributing to clinical brain injury. This review summarizes more recent data suggesting that subtle cardiac dysfunction or low normal levels of cardiac function, as quantified by cardiac output, are related to cognitive and neuroimaging markers of abnormal brain aging in the absence of heart failure or severe cardiomyopathy. Additional work is required, but such associations suggest that reduced cardiac output may be a risk factor for Alzheimer's disease (AD) and abnormal brain aging through the propagation or exacerbation of neurovascular processes, microembolism due to thrombosis, and AD neuropathological processes. Such mechanistic pathways are discussed in the context of a theoretical model that posits a direct pathway of injury between cardiac output and abnormal brain aging (i.e., reduced systemic blood flow disrupts cerebral blood flow homeostasis), contributing to clinical brain injury, independent of shared risk factors for both cardiac dysfunction and abnormal brain aging.
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