BACKGROUND: Stroke risk factors have been increasingly implicated in the development of age-related cognitive decline, the spectrum of vascular cognitive impairment, and, more recently, Alzheimer's disease (AD). In addition, depression and the apolipoprotein (APOE) epsilon4 allele have been reported to influence the association between stroke risk and cognition. However, few studies have described the relations among stroke risk, cognition, and APOE genotype in AD, and the findings have been equivocal. METHODS: Thirty cognitively normal older adults, 30 AD patients with depression, and 30 AD patients without depression were administered a comprehensive neuropsychological battery measuring several domains including memory, attention, language, visuospatial skills, executive functions, and speed of information processing. The Framingham Stroke Risk Profile (FSRP), a validated scale that was developed to predict 10-year probability of stroke, was used to quantify stroke risk burden. RESULTS: AD patients with depression demonstrated greater stroke risk burden relative to the cognitively normal group and, across all participants, increased stroke risk was associated with poorer performance on memory and processing speed measures. Moreover, stroke risk accurately predicted AD diagnosis. Notably, there were no significant differences in stroke risk or cognitive performance between the AD participants with depression and those without depression. CONCLUSION: Given that many markers of stroke risk are modifiable or treatable, our findings have implications for assessment, prevention, and treatment of cognitive decline.
BACKGROUND:Stroke risk factors have been increasingly implicated in the development of age-related cognitive decline, the spectrum of vascular cognitive impairment, and, more recently, Alzheimer's disease (AD). In addition, depression and the apolipoprotein (APOE) epsilon4 allele have been reported to influence the association between stroke risk and cognition. However, few studies have described the relations among stroke risk, cognition, and APOE genotype in AD, and the findings have been equivocal. METHODS: Thirty cognitively normal older adults, 30 ADpatients with depression, and 30 ADpatients without depression were administered a comprehensive neuropsychological battery measuring several domains including memory, attention, language, visuospatial skills, executive functions, and speed of information processing. The Framingham Stroke Risk Profile (FSRP), a validated scale that was developed to predict 10-year probability of stroke, was used to quantify stroke risk burden. RESULTS:ADpatients with depression demonstrated greater stroke risk burden relative to the cognitively normal group and, across all participants, increased stroke risk was associated with poorer performance on memory and processing speed measures. Moreover, stroke risk accurately predicted AD diagnosis. Notably, there were no significant differences in stroke risk or cognitive performance between the ADparticipants with depression and those without depression. CONCLUSION: Given that many markers of stroke risk are modifiable or treatable, our findings have implications for assessment, prevention, and treatment of cognitive decline.
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