Vascular Imaging Abnormalities and Cognition: Mediation by Cortical Volume in Nondemented Individuals: XXXX Risk in Communities-Neurocognitive Study.

@entity1 @entity75 @entity1188 @entity731 @entity62
BACKGROUND AND PURPOSE: The relationships between @entity75 visible on imaging and cognition are complex. We explored the possibility that the cerebral cortical volume mediated these relationships. METHODS: Total of 1906 nondemented @entity1 (59% @entity1 ; 25% African-American; mean age, 76.6 years) in the @entity731 Risk in Communities (ARIC) study underwent cognitive assessments, risk factor assessments, and quantitative MRI for @entity62 ( @entity62 ) and @entity1188 . The Freesurfer imaging analysis pipeline was used to determine regional cerebral volumes. We examined the associations of cognitive domain outcomes with cerebral volumes (hippocampus and separate groups of posterior and frontal cortical regions of interest) and cerebrovascular imaging features (presence of large or small cortical/subcortical @entity1188 and @entity62 volume). We performed mediation pathway analyses to assess the hypothesis that hippocampal and cortical volumes mediated the associations between cerebrovascular imaging features and cognition. RESULTS: In unmediated analyses, @entity62 and @entity1188 were both associated with worse psychomotor speed/executive function. In mediation analyses, @entity62 and @entity1188 associations on psychomotor speed/executive function were significantly attenuated, but not abolished, by the inclusion of the posterior cortical regions of interest volume in the models, and the @entity1188 on psychomotor speed/executive function association were attenuated, but not abolished, by inclusion of the frontal cortical regions of interest volume. CONCLUSIONS: Both @entity62 and @entity1188 were associated with cortical volume, and both lesions were also associated with cognitive performance, implying shared pathophysiological mechanisms. Although cross-sectional, our findings suggest that @entity62 and @entity1188 could be proxies for clinically covert processes that directly damage cortical regions. Microinfarcts are 1 candidate for such a clinically covert process.
