Title | Vascular imaging abnormalities and cognition: mediation by cortical volume in nondemented individuals: atherosclerosis risk in communities-neurocognitive study. |
Publication Type | Journal Article |
Year of Publication | 2015 |
Authors | Knopman DS, Griswold ME, Lirette ST, Gottesman RF, Kantarci K, Sharrett ARichey, Jack CR, Graff-Radford J, Schneider ALC, B Windham G, Coker LH, Albert MS |
Secondary Authors | Mosley TH |
Corporate Authors | ARIC Neurocognitive Investigators |
Journal | Stroke |
Volume | 46 |
Issue | 2 |
Pagination | 433-40 |
Date Published | 2015 Feb |
ISSN | 1524-4628 |
Keywords | Aged, Aged, 80 and over, Atherosclerosis, Cerebrovascular Disorders, Cognition Disorders, Cohort Studies, Female, Humans, Male, Neuropsychological Tests, Residence Characteristics, Risk Factors |
Abstract | BACKGROUND AND PURPOSE: The relationships between cerebrovascular lesions visible on imaging and cognition are complex. We explored the possibility that the cerebral cortical volume mediated these relationships. METHODS: Total of 1906 nondemented participants (59% women; 25% African-American; mean age, 76.6 years) in the Atherosclerosis Risk in Communities (ARIC) study underwent cognitive assessments, risk factor assessments, and quantitative MRI for white matter hyperintensities (WMH) and infarcts. 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 infarcts and WMH 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, WMH and infarcts were both associated with worse psychomotor speed/executive function. In mediation analyses, WMH and infarct 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 infarcts on psychomotor speed/executive function association were attenuated, but not abolished, by inclusion of the frontal cortical regions of interest volume. CONCLUSIONS: Both WMH and infarcts 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 WMH and infarcts could be proxies for clinically covert processes that directly damage cortical regions. Microinfarcts are 1 candidate for such a clinically covert process. |
DOI | 10.1161/STROKEAHA.114.007847 |
Alternate Journal | Stroke |
PubMed ID | 25563642 |
PubMed Central ID | PMC4308430 |
Grant List | HHSN268201100012C / HL / NHLBI NIH HHS / United States HHSN268201100009I / HL / NHLBI NIH HHS / United States HL096899 / HL / NHLBI NIH HHS / United States U01 HL096812 / HL / NHLBI NIH HHS / United States HHSN268201100010C / HL / NHLBI NIH HHS / United States HL096902 / HL / NHLBI NIH HHS / United States HHSN268201100008C / HL / NHLBI NIH HHS / United States HHSN268201100005G / HL / NHLBI NIH HHS / United States U01 HL096917 / HL / NHLBI NIH HHS / United States HHSN268201100008I / HL / NHLBI NIH HHS / United States HHSN268201100007C / HL / NHLBI NIH HHS / United States HL096917 / HL / NHLBI NIH HHS / United States HHSN268201100011I / HL / NHLBI NIH HHS / United States HHSN268201100011C / HL / NHLBI NIH HHS / United States U01 HL096902 / HL / NHLBI NIH HHS / United States HHSN268201100006C / HL / NHLBI NIH HHS / United States R01-HL70825 / HL / NHLBI NIH HHS / United States HL096814 / HL / NHLBI NIH HHS / United States HHSN268201100005I / HL / NHLBI NIH HHS / United States U01 HL096814 / HL / NHLBI NIH HHS / United States HHSN268201100009C / HL / NHLBI NIH HHS / United States R01 HL070825 / HL / NHLBI NIH HHS / United States HHSN268201100005C / HL / NHLBI NIH HHS / United States U01 HL096899 / HL / NHLBI NIH HHS / United States HHSN268201100007I / HL / NHLBI NIH HHS / United States |