The overarching goal of the parent RO1 is to identify the cognitive mechanisms and neural structures that underlie the decline in executive functioning observed in aging. Our working model is that age-associated frontal atrophy, frontal hypoperfusion, and loss of white matter integrity interact to affect information processing speed and executive function. The parent RO1 is prospectively studying 180 normal elderly with structural neuroimaging, perfusion, and cognitive measures at baseline and again after 30-36 months.
The specific aim of this competing revision is to add a fasting blood draw at the follow-up assessments to obtain quantitative laboratory measures of inflammation and vascular risk. While the parent RO1 is designed to assess the impact of age and lifestyle on brain structure and cognition, there are no procedures to collect key data on biological mechanisms that potentially mediate these relationships. It is increasingly clear that inflammation and vascular risk are highly important factors in cognitive aging, even in the absence of neurodegenerative disease. A clearer delineation of how laboratory measures of inflammation and vascular risk interact with brain structure and cognition will significantly advance our understanding of the mechanisms underlying age-related cognitive change and will directly lead to targeted interventions.
This Competing Revision proposes to add a fasting blood draw at the follow-up assessments to obtain quantitative laboratory measures of inflammation and vascular risk on a cohort of 180 functionally normal elderly. This additional biological information, when combined with the parent RO1's lifestyle and health variables, neuroimaging data, and cognitive measures, will enable us to address specific questions about the mechanisms underlying age-related cognitive change.
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