Interaction of Alzheimer Disease and Traumatic Brain Injury on Cortical Thickness.

Autor:	D'Souza GM; Institute of Medical Science, University of Toronto.; Keenan Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St Michael's Hospital, Unity Health Toronto., Churchill NW; Keenan Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St Michael's Hospital, Unity Health Toronto.; Neuroscience Research Program, St. Michael's Hospital.; Physics Department, Toronto Metropolitan University., Guan DX; Cumming School of Medicine, University of Calgary, Calgary, AB, Canada., Khoury MA; Institute of Medical Science, University of Toronto.; Keenan Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St Michael's Hospital, Unity Health Toronto., Graham SJ; Departments of Medical Biophysics.; Physical Sciences Platform, Sunnybrook Research Institute.; Hurvitz Brain Sciences Program, Sunnybrook Research Institute., Kumar S; Institute of Medical Science, University of Toronto.; Psychiatry.; Centre for Addiction and Mental Health, Toronto, ON., Fischer CE; Institute of Medical Science, University of Toronto.; Psychiatry.; Keenan Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St Michael's Hospital, Unity Health Toronto., Schweizer TA; Institute of Medical Science, University of Toronto.; Department of Surgery, Division of Neurosurgery.; Keenan Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St Michael's Hospital, Unity Health Toronto.; Neuroscience Research Program, St. Michael's Hospital.
Jazyk:	angličtina
Zdroj:	Alzheimer disease and associated disorders [Alzheimer Dis Assoc Disord] 2024 Jan-Mar 01; Vol. 38 (1), pp. 14-21. Date of Electronic Publication: 2024 Jan 29.
DOI:	10.1097/WAD.0000000000000607
Abstrakt:	Introduction: Traumatic brain injury (TBI) is associated with an accelerated course of dementia, although biological relationships are incompletely understood. Methods: The study examined 1124 participants, including 343 with Alzheimer disease (AD), 127 with AD with TBI, 266 cognitively normal adults with TBI, and 388 cognitively normal adults without TBI. Cortical thickness was quantified from T1-weighted magnetic resonance imaging data. Multiple linear regression was used to determine the interaction between AD and TBI on cortical thickness. Results: Among those with AD, TBI was associated with an earlier age of AD onset but, counterintuitively, less cortical thinning in frontotemporal regions relative to non-AD controls. Discussion: AD with TBI represents a distinct group from AD, likely with distinct pathologic contributions beyond gray matter loss. This finding has important implications for the diagnosis and treatment of AD in the presence of TBI and indicates that models of AD, aging, and neural loss should account for TBI history. Competing Interests: The authors declare no conflicts of interest. (Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc.)
Databáze:	MEDLINE
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