{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,8]],"date-time":"2026-10-08T21:57:33Z","timestamp":1791496653697,"version":"4.3.4"},"reference-count":56,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2021,12,20]],"date-time":"2021-12-20T00:00:00Z","timestamp":1639958400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Euro J of Neurology"],"published-print":{"date-parts":[[2022,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and purpose<\/jats:title>\n                    <jats:p>The faster rates of cognitive decline and predominance of atypical forms in early\u2010onset Alzheimer's disease (EOAD) suggest that neuropsychiatric symptoms could be different in EOAD compared to late\u2010onset AD (LOAD); however, prior studies based on non\u2010biomarker\u2010diagnosed cohorts show discordant results. Our goal was to determine the profile of neuropsychiatric symptoms in EOAD and LOAD, in a cohort with biomarker\/postmortem\u2010confirmed diagnoses. Additionally, the contribution of co\u2010pathologies was explored.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>In all, 219 participants (135 EOAD, 84 LOAD) meeting National Institute on Aging and Alzheimer's Association criteria for AD (115 amyloid positron emission tomography\/cerebrospinal fluid biomarkers, 104 postmortem diagnosis) at the University of California San Francisco were evaluated. The Neuropsychiatric Inventory\u2014Questionnaire (NPI\u2010Q) was assessed at baseline and during follow\u2010up. The NPI\u2010Q mean comparisons and regression models adjusted by cognitive (Mini\u2010Mental State Examination) and functional status (Clinical Dementia Rating Sum of Boxes) were performed to determine the effect of EOAD\/LOAD and amnestic\/non\u2010amnestic diagnosis on NPI\u2010Q. Regression models assessing the effect of co\u2010pathologies on NPI\u2010Q were performed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      At baseline, the NPI\u2010Q scores were higher in EOAD compared to LOAD (\n                      <jats:italic>p\u00a0<\/jats:italic>\n                      &lt;\u00a00.05). Longitudinally, regression models showed a significant effect of diagnosis, where EOAD had higher NPI\u2010Q total, anxiety, motor disturbances and night\u2010time behavior scores (\n                      <jats:italic>p\u00a0<\/jats:italic>\n                      &lt;\u00a00.05). No differences between amnestics\/non\u2010amnestics were found. Argyrophilic grain disease co\u2010pathology predicted a higher severity of NPI\u2010Q scores in LOAD.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Anxiety, night\u2010time behaviors and motor disturbances are more severe in EOAD than LOAD across the disease course. The differential patterns of neuropsychiatric symptoms observed between EOAD\/LOAD could suggest a pattern of selective vulnerability extending to the brain's subcortical structures. Further, co\u2010pathologies such as argyrophilic grain disease in LOAD may also play a role in increasing neuropsychiatric symptoms.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/ene.15203","type":"journal-article","created":{"date-parts":[[2021,12,4]],"date-time":"2021-12-04T08:05:26Z","timestamp":1638605126000},"page":"957-967","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":38,"title":["The severity of neuropsychiatric symptoms is higher in early\u2010onset than late\u2010onset Alzheimer\u2019s disease"],"prefix":"10.1111","volume":"29","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3404-2765","authenticated-orcid":false,"given":"Neus","family":"Falg\u00e0s","sequence":"first","affiliation":[{"name":"Department of Neurology, Memory and Aging Center Weill Institute for Neurosciences University of California San Francisco California USA"},{"name":"Global Brain Health Institute University of California San Francisco California USA"},{"name":"Alzheimer\u2019s Disease and Other Cognitive Disorders Unit Hospital Cl\u00ednic de Barcelona. 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