Stroke is a leading cause of morbidity and mortality, and is common in older persons. Strokes can cause a range of neurologic symptoms depending on location, but how they impact memory and other specific cognitive functions over time in healthy older persons is not clear. In this paper, Reitz and colleagues studied whether stroke was associated with decline in memory and other cognitive functions in a group of older persons without dementia. Using a cohort of over 1,000 older persons from northern Manhattan, New York, the authors followed subjects over a 5-year period. They found that persons with evidence of stroke had more rapid decline in memory over the ensuing 5 years compared to those without stroke. Men had greater memory decline after stroke compared to women, and persons without an ApoE4 genotype had greater memory decline after stroke compared to persons with an ApoE4 genotype.
This study highlights the important role of vascular disease in the spectrum of cognitive impairment and dementia in older persons, and like other recent studies, suggests that memory loss in older persons can be associated with both neurodegenerative and vascular pathology. As noted by the authors, there are several mechanisms by which strokes may worsen cognitive function. One possibility is a direct effect of tissue damage; however, the authors did not have information of the location of cerebrovascular disease. While this remains a consideration, the strong effect of stroke on memory suggests a possible role for concomitant Alzheimer disease. Indeed, cerebral infarctions have been shown in several clinical-pathologic studies to lower the threshold for the clinical expression of Alzheimer disease pathology. Whether this is an additive effect of two unrelated pathologies, or cerebral infarction and Alzheimer disease are linked by a common cause or act in synergy to worsen memory function will be important to explore in future studies.
Interestingly, not all persons in this study exhibited equal risk for memory decline after stroke. The different risk profiles by gender and ApoE genotype may implicate an additional role for hormonal, biochemical, or other factors which may protect the brain from injury. It will be important to further explore these and other risk factors and the mechanism by which the brain may protect itself from the evolution of memory problems, whether by vascular disease or Alzheimer disease, or both.
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Rush Alzheimer's Disease Center
Stroke is a leading cause of morbidity and mortality, and is common in older persons. Strokes can cause a range of neurologic symptoms depending on location, but how they impact memory and other specific cognitive functions over time in healthy older persons is not clear. In this paper, Reitz and colleagues studied whether stroke was associated with decline in memory and other cognitive functions in a group of older persons without dementia. Using a cohort of over 1,000 older persons from northern Manhattan, New York, the authors followed subjects over a 5-year period. They found that persons with evidence of stroke had more rapid decline in memory over the ensuing 5 years compared to those without stroke. Men had greater memory decline after stroke compared to women, and persons without an ApoE4 genotype had greater memory decline after stroke compared to persons with an ApoE4 genotype.
This study highlights the important role of vascular disease in the spectrum of cognitive impairment and dementia in older persons, and like other recent studies, suggests that memory loss in older persons can be associated with both neurodegenerative and vascular pathology. As noted by the authors, there are several mechanisms by which strokes may worsen cognitive function. One possibility is a direct effect of tissue damage; however, the authors did not have information of the location of cerebrovascular disease. While this remains a consideration, the strong effect of stroke on memory suggests a possible role for concomitant Alzheimer disease. Indeed, cerebral infarctions have been shown in several clinical-pathologic studies to lower the threshold for the clinical expression of Alzheimer disease pathology. Whether this is an additive effect of two unrelated pathologies, or cerebral infarction and Alzheimer disease are linked by a common cause or act in synergy to worsen memory function will be important to explore in future studies.
Interestingly, not all persons in this study exhibited equal risk for memory decline after stroke. The different risk profiles by gender and ApoE genotype may implicate an additional role for hormonal, biochemical, or other factors which may protect the brain from injury. It will be important to further explore these and other risk factors and the mechanism by which the brain may protect itself from the evolution of memory problems, whether by vascular disease or Alzheimer disease, or both.
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