{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T15:07:16Z","timestamp":1790694436373,"version":"4.1.0"},"reference-count":69,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2025,4,25]],"date-time":"2025-04-25T00:00:00Z","timestamp":1745539200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100009192","name":"Alberta Innovates","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100009192","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Gordie Howe CARES"},{"name":"UK National Institute for Health and Care Research Exeter Biomedical Research Centre"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2025,10,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Whether or not neuropsychiatric symptoms (NPS) in advance of dementia are associated with Alzheimer\u2019s disease (AD) and\/or other neurodegenerative dementias remains to be determined. The mild behavioural impairment (MBI) construct selects persons with NPS that are later-life emergent and persistent to identify a high-risk group for cognitive decline and incident dementia. Here, in older adults without dementia at baseline, we examined whether post-mortem AD and other neurodegenerative pathologies were associated with MBI in the 5 years before death.<\/jats:p>\n               <jats:p>National Alzheimer\u2019s Coordinating Center study autopsy participants (n = 1016, 82.6 years of age, 48.7% female, 60% normal cognition) were included in the analyses. Using the Neuropsychiatric Inventory-Questionnaire, MBI+ status was operationalized as NPS persistence at more than two-thirds of pre-dementia study visits; otherwise, status was non-MBI NPS. The presence of AD, Lewy body disease (LBD) and transactive response DNA-binding protein 43 neuropathological changes was determined using published guidelines. Adjusted multinomial logistic regressions modelled pathology\u2013NPS status associations. Adjusted Cox proportional hazards regressions modelled hazard for AD dementia at each NPS status level, including interaction terms with cognitive status and each co-pathology.<\/jats:p>\n               <jats:p>AD+ individuals (51.4%) were 88.4% more likely to be MBI+ \u223c5 years prior than AD\u2212 individuals [odds ratio: 1.88, 95% confidence interval (CI): 1.29\u20132.75, P &amp;lt; 0.01]; however, the likelihood of having non-MBI NPS was not different (odds ratio: 1.22, CI: 0.90\u20131.66, P = 0.20). No significant associations were seen for LBD pathology, even among AD+ participants. There were no significant differences in the levels of LBD or transactive response DNA-binding protein 43 in those with MBI in comparison to no MBI. Among MBI progressors to dementia (n = 106), 33.0% were solely AD+, 18.9% were mixed AD+ and LBD+, and 11.3% had all three pathologies. For all those with MBI (including dementia non-progressors), of persons with LBD, 83.4% were comorbid with AD. In the survival analysis, MBI+ individuals had a 2.03-fold greater progression rate to AD dementia than those without NPS (CI: 1.60\u20132.57, P &amp;lt; 0.01). The progression rate was higher in mild cognitive impairment , but the effect of MBI on progression was greater in normal cognition (hazard ratio: 3.05, CI: 1.37\u20136.80, P &amp;lt; 0.01) versus mild cognitive impairment (hazard ratio: 1.93, CI: 1.51\u20132.47, P &amp;lt; 0.01). Limbic LBD appeared also to moderate the association between MBI and incident AD (limbic LBD+ hazard ratio: 4.64, CI: 2.05\u201310.50, P &amp;lt; 0.001; limbic LBD\u2212 hazard ratio: 1.87, CI: 1.46\u20132.40, P &amp;lt; 0.001).<\/jats:p>\n               <jats:p>Antecedent MBI was strongly associated with AD pathology but not with other neurodegenerative dementias. Inclusion of MBI in research and clinical frameworks for dementia might aid in identification of early stages of neurodegenerative disease, which might be helpful for selecting patients for treatment with AD-modifying drugs.<\/jats:p>","DOI":"10.1093\/brain\/awaf156","type":"journal-article","created":{"date-parts":[[2025,4,25]],"date-time":"2025-04-25T15:48:46Z","timestamp":1745596126000},"page":"3694-3704","source":"Crossref","is-referenced-by-count":18,"title":["Neuropsychiatric symptoms and progression to pathologically confirmed Alzheimer\u2019s disease"],"prefix":"10.1093","volume":"148","author":[{"given":"Sergio F","family":"Sharif","sequence":"first","affiliation":[{"name":"Cumming School of Medicine, University of Calgary , Calgary, AB , T2N 1N4","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7065-1963","authenticated-orcid":false,"given":"Dylan X","family":"Guan","sequence":"additional","affiliation":[{"name":"Cumming School of Medicine, University of Calgary , Calgary, AB , T2N 1N4","place":["Canada"]},{"name":"Hotchkiss Brain Institute, University of Calgary , Calgary, AB , T2N 4Z6","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tamara S","family":"Bodnar","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, University of Calgary , Calgary, AB , T2N 1N4","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffery T","family":"Joseph","sequence":"additional","affiliation":[{"name":"Hotchkiss Brain Institute, University of Calgary , Calgary, AB , T2N 4Z6","place":["Canada"]},{"name":"Department of Pathology and Laboratory Medicine, University of Calgary , Calgary, AB , T2N 4Z6","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3930-4354","authenticated-orcid":false,"given":"Henrik","family":"Zetterberg","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg , M\u00f6lndal 431 39 ,","place":["Sweden"]},{"name":"Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital , M\u00f6lndal 431 39 ,","place":["Sweden"]},{"name":"Department of Neurodegenerative Disease, UCL Institute of Neurology , London WC1N 3BG ,","place":["UK"]},{"name":"UK Dementia Research Institute at UCL , London NW1 3BT ,","place":["UK"]},{"name":"Hong Kong Center for Neurodegenerative Diseases , Clear Water Bay, Hong Kong ,","place":["China"]},{"name":"Wisconsin Alzheimer\u2019s Disease Research Center, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison , Madison, WI 53792 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric E","family":"Smith","sequence":"additional","affiliation":[{"name":"Hotchkiss Brain Institute, University of Calgary , Calgary, AB , T2N 4Z6","place":["Canada"]},{"name":"Department of Community Health Sciences, University of Calgary , Calgary, AB , T2N 4Z6","place":["Canada"]},{"name":"Department of Clinical Neurosciences, University of Calgary , Calgary, AB , T2N 4Z6","place":["Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5529-3731","authenticated-orcid":false,"given":"Zahinoor","family":"Ismail","sequence":"additional","affiliation":[{"name":"Hotchkiss Brain Institute, University of Calgary , Calgary, AB , T2N 4Z6","place":["Canada"]},{"name":"Department of Pathology and Laboratory Medicine, University of Calgary , Calgary, AB , T2N 4Z6","place":["Canada"]},{"name":"Department of Community Health Sciences, University of Calgary , Calgary, AB , T2N 4Z6","place":["Canada"]},{"name":"Department of Clinical Neurosciences, University of Calgary , Calgary, AB , T2N 4Z6","place":["Canada"]},{"name":"O\u2019Brien Institute for Public Health, University of Calgary , Calgary, AB , T2N 4Z6","place":["Canada"]},{"name":"Department of Psychiatry, University of Calgary , Calgary, AB , T2N 4Z6","place":["Canada"]},{"name":"Clinical and Biomedical Sciences, Faculty of Health and Life Sciences, University of Exeter , Exeter EX1 2HZ ,","place":["UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2025,4,25]]},"reference":[{"issue":"1","key":"2025100310364626500_awaf156-B1","doi-asserted-by":"crossref","first-page":"32","DOI":"10.1186\/s13024-019-0333-5","article-title":"The neuropathological diagnosis of Alzheimer\u2019s disease","volume":"14","author":"DeTure","year":"2019","journal-title":"Mol 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for prior psychiatric diagnosis in patients with early neurodegenerative disease","volume":"72","author":"Woolley","year":"2011","journal-title":"J Clin Psychiatry"},{"key":"2025100310364626500_awaf156-B5","doi-asserted-by":"crossref","first-page":"333","DOI":"10.1016\/j.dadm.2019.02.006","article-title":"Time course of neuropsychiatric symptoms and cognitive diagnosis in National Alzheimer\u2019s Coordinating Centers volunteers","volume":"11","author":"Wise","year":"2019","journal-title":"Alzheimers Dement (Amst)"},{"issue":"1","key":"2025100310364626500_awaf156-B6","doi-asserted-by":"crossref","first-page":"56","DOI":"10.14283\/jpad.2023.125","article-title":"CTAD task force paper: Neuropsychiatric symptoms in AD: Clinical trials targeting mild behavioral impairment: A report from the international CTAD task force","volume":"11","author":"Soto","year":"2024","journal-title":"J Prev Alzheimers 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