@article{d50685346e0c47cd8c1f957a0cee07de,
title = "Beta-amyloid moderates the relationship between cortical thickness and attentional control in middle- and older-aged adults",
abstract = "Although often unmeasured in studies of cognition, many older adults possess Alzheimer disease (AD) pathologies such as beta-amyloid (Aβ) deposition, despite being asymptomatic. We were interested in examining whether the behavior-structure relationship observed in later life was altered by the presence of preclinical AD pathology. A total of 511 cognitively unimpaired adults completed magnetic resonance imaging and three attentional control tasks; a subset (n = 396) also underwent Aβ-positron emissions tomography. A vertex-wise model was conducted to spatially represent the relationship between cortical thickness and average attentional control accuracy, while moderation analysis examined whether Aβ deposition impacted this relationship. First, we found that reduced cortical thickness in temporal, medial- and lateral-parietal, and dorsolateral prefrontal cortex, predicted worse performance on the attention task composite. Subsequent moderation analyses observed that levels of Aβ significantly influence the relationship between cortical thickness and attentional control. Our results support the hypothesis that preclinical AD, as measured by Aβ deposition, is partially driving what would otherwise be considered general aging in a cognitively normal adult population.",
keywords = "Alzheimer disease, Amyloid, Attention, Cognition, Control, Free surfer, Moderation",
author = "McKay, {Nicole S.} and Aylin Dincer and Vidushri Mehrotra and Aschenbrenner, {Andrew J.} and David Balota and Hornbeck, {Russ C.} and Jason Hassenstab and Morris, {John C.} and Benzinger, {Tammie L.S.} and Gordon, {Brian A.}",
note = "Funding Information: This work was supported by NIH grants K01AG053474 , P01AG003991 , P50AG005681 , P01AG026276 , R01EB009352 , P30NS098577 . Computations were supported by the facilities of the Washington University Center for High Performance Computing, which were partially funded by NIH grants 1S10RR022984-01A1 and 1S10OD018091-01 . J.C. Morris is funded by NIH grants P30 AG066444 ; P01AG003991 ; P01AG026276 ; U19 AG032438 ; and U19 AG024904 . Funding Information: T.L.S. Benzinger: investigator-initiated research funding from the NIH, the Alzheimer's Association, the Barnes-Jewish Hospital Foundation and Avid Radiopharmaceuticals (a wholly owned subsidiary of Eli Lilly). She participates as a site investigator in clinical trials sponsored by Avid Radiopharmaceuticals, Eli Lilly, Biogen, Eisai, Jaansen, and Roche. She serves as an unpaid consultant to Eisai and Siemens. She is on the Speaker's Bureau for Biogen. Neither Dr. Morris nor his family owns stock or has equity interest (outside of mutual funds or other externally directed accounts) in any pharmaceutical or biotechnology company. No other disclosures to declare. Publisher Copyright: {\textcopyright} 2022 Elsevier Inc.",
year = "2022",
month = apr,
doi = "10.1016/j.neurobiolaging.2021.12.012",
language = "English",
volume = "112",
pages = "181--190",
journal = "Neurobiology of Aging",
issn = "0197-4580",
}