{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T01:34:18Z","timestamp":1787794458912,"version":"build-2784847793"},"reference-count":27,"publisher":"American Medical Association (AMA)","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAMA Neurol"],"published-print":{"date-parts":[[2025,6,1]]},"abstract":"\n Importance<\/jats:title>\n The defining pathological features of Alzheimer disease (AD) may also be contributing factors in other dementias.<\/jats:p>\n <\/jats:sec>\n \n Objective<\/jats:title>\n To examine the prevalence of \u03b2-amyloid (A\u03b2) and tau pathophysiological changes as indicated by cerebrospinal fluid biomarkers, as well as their association with clinical disease progression, across a broad range of dementias.<\/jats:p>\n <\/jats:sec>\n \n Design, Setting, and Participants<\/jats:title>\n In this cross-sectional study with a duration of 12 years (October 5, 2010, to August 31, 2022), clinical data from the Swedish registry for cognitive disorders and dementia (SveDem) were merged with clinical routine biomarker measurements of the core cerebrospinal fluid biomarkers of AD: A\u03b21-42, total tau (t-tau), and phosphorylated tau 181 (p-tau181). Participants were individuals with a dementia diagnosis who had a complete set of cerebrospinal fluid A\u03b21-42, t-tau, and p-tau measurements registered less than 3 years after the date of diagnosis. Data were analyzed from April to November 2023.<\/jats:p>\n <\/jats:sec>\n \n Exposures<\/jats:title>\n Age, sex, and dementia diagnosis.<\/jats:p>\n <\/jats:sec>\n \n Main Outcomes and Measures<\/jats:title>\n Biomarker profiles in relation to diagnosis and cognitive status as indicated by Mini-Mental State Examination (MMSE) scores.<\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n Among 15\u202f004 individuals with a dementia diagnosis in the SveDem database, 13\u202f882 were included in this study (7328 females [53%], 6554 males [47%]; median [IQR] age, 74 [68-79] years). Apart from the AD groups (early-onset AD, 1150 [68%]; late-onset AD, 3392 [65%]; mixed AD and vascular dementia, 1038 [52%]), the dementia not otherwise specified group had the most patients (443 [25%]) with a clear AD-like biomarker profile, while Parkinson disease dementia and the frontotemporal dementia groups had the smallest shares (15 [9%] and 51 [8%], respectively). MMSE score was associated with cerebrospinal fluid A\u03b21-42 in late-onset AD, vascular dementia, frontotemporal dementia, and dementia not otherwise specified; with t-tau in late-onset AD, early-onset AD, and dementia not otherwise specified; and with p-tau181 in early-onset AD.<\/jats:p>\n <\/jats:sec>\n \n Conclusions and Relevance<\/jats:title>\n A\u03b2-related pathology is a defining feature of AD, and most patients clinically diagnosed with AD have biomarker evidence of this process, but the same is found in other dementias, although less commonly. Cerebrospinal fluid biomarker concentrations of AD-like pathology were associated with cognitive function but mainly in patients with an AD-related diagnosis (early- and late-onset AD).<\/jats:p>\n <\/jats:sec>","DOI":"10.1001\/jamaneurol.2025.0693","type":"journal-article","created":{"date-parts":[[2025,4,28]],"date-time":"2025-04-28T11:31:52Z","timestamp":1745839912000},"page":"580","source":"Crossref","is-referenced-by-count":17,"title":["Cerebrospinal Fluid Biomarkers for Alzheimer Disease Among Patients With Dementia"],"prefix":"10.1001","volume":"82","author":[{"given":"Tobias Borgh","family":"Skillb\u00e4ck","sequence":"first","affiliation":[{"name":"Region V\u00e4stra G\u00f6taland, Department of Neuropsychiatry, Sahlgrenska University Hospital, M\u00f6lndal, Sweden"},{"name":"Neuropsychiatric Epidemiology Unit, Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, Centre for Ageing and Health (AgeCap) at the University of Gothenburg, Gothenburg, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linus","family":"J\u00f6nsson","sequence":"additional","affiliation":[{"name":"Division of Neurogeriatrics, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ingmar","family":"Skoog","sequence":"additional","affiliation":[{"name":"Region V\u00e4stra G\u00f6taland, Department of Neuropsychiatry, Sahlgrenska University Hospital, M\u00f6lndal, Sweden"},{"name":"Neuropsychiatric Epidemiology Unit, Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy, Centre for Ageing and Health (AgeCap) at the University of Gothenburg, Gothenburg, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaj","family":"Blennow","sequence":"additional","affiliation":[{"name":"Region V\u00e4stra G\u00f6taland, Department of Neuropsychiatry, Sahlgrenska University Hospital, M\u00f6lndal, Sweden"},{"name":"Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, M\u00f6lndal, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria","family":"Eriksdotter","sequence":"additional","affiliation":[{"name":"Division of Clinical Geriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden"},{"name":"Theme Inflammation and Aging, Karolinska University Hospital, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henrik","family":"Zetterberg","sequence":"additional","affiliation":[{"name":"Region V\u00e4stra G\u00f6taland, Department of Neuropsychiatry, Sahlgrenska University Hospital, M\u00f6lndal, Sweden"},{"name":"Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, M\u00f6lndal, Sweden"},{"name":"Department of Neurodegenerative Disease, UCL Institute of 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