Cognitive and Anatomic Contributions of Metabolic Decline in Alzheimer Disease and Cerebrovascular Disease

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Abstract
Dementia in older adults is frequently caused by the combined pathologic conditions of Alzheimer disease (AD) and cerebrovascular disease (CVD). Since AD and CVD frequently occur together and overlap in their presentations, their differentiation may be difficult or impossible in a given case of dementia. Nevertheless, there is ample evidence that they contribute separately to the development of cognitive decline and dementia.1,2 We, therefore, approached this study with the goal of defining the different pathways through which AD and CVD exert their effects on brain structure and function. While this approach is unlikely to lead to the development of diagnostic tests for the 2 conditions, it may elucidate how dementia occurs through their differential pathological vulnerabilities. Both cross-sectional and longitudinal relationships were of interest. We proposed that hippocampal volume (HV) and memory loss would primarily contribute to temporoparietalhypometabolism, while white matter hyperintensities (WMH) and executive dysfunction would contribute to frontal hypometabolism. Our goal was to define the patterns of association between these anatomic and cognitive variables with cross-sectional and longitudinal changes in glucose metabolism to explain how different brain systems are susceptible to the different pathological processes of AD and CVD.