Neurological research · 2006
How do heart disease and stroke become risk factors for Alzheimer's disease?
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de la Torre Jack C
Аннотация
BACKGROUND: Heart disease and stroke are two of the major leading causes of death and disability in the world. Mainly affecting the elderly population, heart disease and stroke are important risk factors for Alzheimer's disease (AD).
METHODS: This review examines the evidence linking chronic brain hypoperfusion (CBH) produced by several types of heart disease and stroke on the development of AD.
RESULTS: The evidence indicates a strong association between such risk factors as coronary artery bypass surgery (CABG), atrial fibrillation, aortic/mitral valve damage, hypertension, hypotension, congestive heart failure, cerebrovascular-carotid atherosclerosis, and transient ischemic attacks in producing CBH. In people whose cerebral perfusion is already diminished by their advanced age, further cerebral blood flow reductions from heart-brain vascular-related risk factors, seemingly increases the probability of AD. The evidence also suggests that a neuronal energy crisis brought on by a relentless CBH is responsible for protein synthesis defects that later result in the classic AD neurodegenerative lesions such as the formation of excess beta-amyloid plaques and neurofibrillary tangles.
CONCLUSIONS: Knowledge of how heart disease and stroke can progress to AD should provide a better understanding of the physiopathology characteristic of AD and also target more precise therapy in preventing, controlling or reversing this dementia.
METHODS: This review examines the evidence linking chronic brain hypoperfusion (CBH) produced by several types of heart disease and stroke on the development of AD.
RESULTS: The evidence indicates a strong association between such risk factors as coronary artery bypass surgery (CABG), atrial fibrillation, aortic/mitral valve damage, hypertension, hypotension, congestive heart failure, cerebrovascular-carotid atherosclerosis, and transient ischemic attacks in producing CBH. In people whose cerebral perfusion is already diminished by their advanced age, further cerebral blood flow reductions from heart-brain vascular-related risk factors, seemingly increases the probability of AD. The evidence also suggests that a neuronal energy crisis brought on by a relentless CBH is responsible for protein synthesis defects that later result in the classic AD neurodegenerative lesions such as the formation of excess beta-amyloid plaques and neurofibrillary tangles.
CONCLUSIONS: Knowledge of how heart disease and stroke can progress to AD should provide a better understanding of the physiopathology characteristic of AD and also target more precise therapy in preventing, controlling or reversing this dementia.