Avron Spiro1, Christopher B Brady. 1. Massachusetts Veterans Epidemiology Research and Information Center, VA Boston Healthcare System, Massachusetts, USA. aspiro3@bu.edu
Abstract
OBJECTIVES: We argue that age is a descriptive, and not explanatory, variable and consequently cannot account for the cognitive changes that often occur with aging. Once age is removed from consideration, other truly causal explanations for "cognitive aging" must be identified. We argue that health and disease represent an important class of explanatory variables for age-related cognitive changes. METHODS/ RESULTS: We make this argument first by reviewing the prevalence of risk factors, disability, and subclinical and frank disease in the elderly population. We emphasize that the complexity of health effects rivals that of age on cognition while noting that most studies of cognitive aging rarely consider this complexity fully. We then consider in more detail the "vascular hypothesis," which proposes that vascular diseases (e.g., stroke, heart disease) and their risk factors (e.g., hypertension) can explain aspects of cognitive decline in aging through their impact on circulatory and brain functions. Clinical implications of this hypothesis suggest that treatment of vascular risk factors might well reduce the incidence or severity of dementia syndromes. DISCUSSION: We conclude with a brief summary of approaches to further integrate aspects of health and disease into the study of "cognitive aging."
OBJECTIVES: We argue that age is a descriptive, and not explanatory, variable and consequently cannot account for the cognitive changes that often occur with aging. Once age is removed from consideration, other truly causal explanations for "cognitive aging" must be identified. We argue that health and disease represent an important class of explanatory variables for age-related cognitive changes. METHODS/ RESULTS: We make this argument first by reviewing the prevalence of risk factors, disability, and subclinical and frank disease in the elderly population. We emphasize that the complexity of health effects rivals that of age on cognition while noting that most studies of cognitive aging rarely consider this complexity fully. We then consider in more detail the "vascular hypothesis," which proposes that vascular diseases (e.g., stroke, heart disease) and their risk factors (e.g., hypertension) can explain aspects of cognitive decline in aging through their impact on circulatory and brain functions. Clinical implications of this hypothesis suggest that treatment of vascular risk factors might well reduce the incidence or severity of dementia syndromes. DISCUSSION: We conclude with a brief summary of approaches to further integrate aspects of health and disease into the study of "cognitive aging."
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