Cassandra Marotta, Fernando Gonzalez-Ortiz, Michael Turton, Henrik Zetterberg, Peter Harrison, Christopher M Hovens, Benjamin Sinclair, Terence J O'Brien, Kaj Blennow, Lucy Vivash
{"title":"脑源性tau测量阿尔茨海默病和额颞叶痴呆的治疗效果。","authors":"Cassandra Marotta, Fernando Gonzalez-Ortiz, Michael Turton, Henrik Zetterberg, Peter Harrison, Christopher M Hovens, Benjamin Sinclair, Terence J O'Brien, Kaj Blennow, Lucy Vivash","doi":"10.1002/dad2.70123","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Brain-derived tau (BD-tau) measures tau specifically from brain-derived sources and can differentiate Alzheimer's disease (AD) from other diseases. This study investigated BD-tau as a potential biomarker of treatment effect.</p><p><strong>Methods: </strong>BD-tau and phosphorylated tau-217 (p-tau217) levels were measured after treatment with an anti-tau drug in AD and behavioral variant frontotemporal dementia (bvFTD) clinical trials, and the association with total tau (t-tau), p-tau181<sub>,</sub> and amyloid beta 42 (Aβ42) was examined.</p><p><strong>Results: </strong>Cerebrospinal fluid (CSF) BD-tau decreased after treatment in the AD cohort; however, no change was seen in bvFTD or p-tau217 in either cohort. CSF t-tau and p-tau181 correlated with BD-tau in AD (<i>r</i> = 0.9113 and 0.7746, <i>p</i> < 0.0001) and bvFTD (<i>r</i> = 1.0 and <i>r</i> = 0.79, <i>p</i> < 0.05). CSF BD-tau did not correlate with serum or plasma BD-tau in bvFTD.</p><p><strong>Discussion: </strong>CSF BD-tau shows potential as a biomarker of treatment effect in AD but not bvFTD. Further research is needed to investigate this effect in blood-based samples and in other neurodegenerative diseases. <b>Trial registration</b>: ACTRN12611001200976, ACTRN12617001218381.</p><p><strong>Highlights: </strong>Cerebrospinal fluid (CSF) brain-derived tau (BD-tau) levels decreased with sodium selenate treatment in patients with Alzheimer's disease (AD).CSF BD-tau levels did not change with sodium selenate treatment in bvFTD.Baseline CSF BD-tau correlated with CSF total tau (t-tau) and phosphorylated tau-181 (p-tau181) in AD and behavioral variant frontotemporal dementia (bvFTD).Baseline serum and plasma BD-tau levels did not correlate with CSF BD-tau in bvFTD.CSF p-tau217 did not change with sodium selenate treatment in AD or bvFTD.</p>","PeriodicalId":53226,"journal":{"name":"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring","volume":"17 2","pages":"e70123"},"PeriodicalIF":4.4000,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12140970/pdf/","citationCount":"0","resultStr":"{\"title\":\"Brain-derived tau to measure treatment effect in Alzheimer's disease and frontotemporal dementia.\",\"authors\":\"Cassandra Marotta, Fernando Gonzalez-Ortiz, Michael Turton, Henrik Zetterberg, Peter Harrison, Christopher M Hovens, Benjamin Sinclair, Terence J O'Brien, Kaj Blennow, Lucy Vivash\",\"doi\":\"10.1002/dad2.70123\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Introduction: </strong>Brain-derived tau (BD-tau) measures tau specifically from brain-derived sources and can differentiate Alzheimer's disease (AD) from other diseases. This study investigated BD-tau as a potential biomarker of treatment effect.</p><p><strong>Methods: </strong>BD-tau and phosphorylated tau-217 (p-tau217) levels were measured after treatment with an anti-tau drug in AD and behavioral variant frontotemporal dementia (bvFTD) clinical trials, and the association with total tau (t-tau), p-tau181<sub>,</sub> and amyloid beta 42 (Aβ42) was examined.</p><p><strong>Results: </strong>Cerebrospinal fluid (CSF) BD-tau decreased after treatment in the AD cohort; however, no change was seen in bvFTD or p-tau217 in either cohort. CSF t-tau and p-tau181 correlated with BD-tau in AD (<i>r</i> = 0.9113 and 0.7746, <i>p</i> < 0.0001) and bvFTD (<i>r</i> = 1.0 and <i>r</i> = 0.79, <i>p</i> < 0.05). CSF BD-tau did not correlate with serum or plasma BD-tau in bvFTD.</p><p><strong>Discussion: </strong>CSF BD-tau shows potential as a biomarker of treatment effect in AD but not bvFTD. Further research is needed to investigate this effect in blood-based samples and in other neurodegenerative diseases. <b>Trial registration</b>: ACTRN12611001200976, ACTRN12617001218381.</p><p><strong>Highlights: </strong>Cerebrospinal fluid (CSF) brain-derived tau (BD-tau) levels decreased with sodium selenate treatment in patients with Alzheimer's disease (AD).CSF BD-tau levels did not change with sodium selenate treatment in bvFTD.Baseline CSF BD-tau correlated with CSF total tau (t-tau) and phosphorylated tau-181 (p-tau181) in AD and behavioral variant frontotemporal dementia (bvFTD).Baseline serum and plasma BD-tau levels did not correlate with CSF BD-tau in bvFTD.CSF p-tau217 did not change with sodium selenate treatment in AD or bvFTD.</p>\",\"PeriodicalId\":53226,\"journal\":{\"name\":\"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring\",\"volume\":\"17 2\",\"pages\":\"e70123\"},\"PeriodicalIF\":4.4000,\"publicationDate\":\"2025-06-05\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12140970/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1002/dad2.70123\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/4/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q1\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Alzheimer''s and Dementia: Diagnosis, Assessment and Disease Monitoring","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/dad2.70123","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/4/1 0:00:00","PubModel":"eCollection","JCR":"Q1","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
Brain-derived tau to measure treatment effect in Alzheimer's disease and frontotemporal dementia.
Introduction: Brain-derived tau (BD-tau) measures tau specifically from brain-derived sources and can differentiate Alzheimer's disease (AD) from other diseases. This study investigated BD-tau as a potential biomarker of treatment effect.
Methods: BD-tau and phosphorylated tau-217 (p-tau217) levels were measured after treatment with an anti-tau drug in AD and behavioral variant frontotemporal dementia (bvFTD) clinical trials, and the association with total tau (t-tau), p-tau181, and amyloid beta 42 (Aβ42) was examined.
Results: Cerebrospinal fluid (CSF) BD-tau decreased after treatment in the AD cohort; however, no change was seen in bvFTD or p-tau217 in either cohort. CSF t-tau and p-tau181 correlated with BD-tau in AD (r = 0.9113 and 0.7746, p < 0.0001) and bvFTD (r = 1.0 and r = 0.79, p < 0.05). CSF BD-tau did not correlate with serum or plasma BD-tau in bvFTD.
Discussion: CSF BD-tau shows potential as a biomarker of treatment effect in AD but not bvFTD. Further research is needed to investigate this effect in blood-based samples and in other neurodegenerative diseases. Trial registration: ACTRN12611001200976, ACTRN12617001218381.
Highlights: Cerebrospinal fluid (CSF) brain-derived tau (BD-tau) levels decreased with sodium selenate treatment in patients with Alzheimer's disease (AD).CSF BD-tau levels did not change with sodium selenate treatment in bvFTD.Baseline CSF BD-tau correlated with CSF total tau (t-tau) and phosphorylated tau-181 (p-tau181) in AD and behavioral variant frontotemporal dementia (bvFTD).Baseline serum and plasma BD-tau levels did not correlate with CSF BD-tau in bvFTD.CSF p-tau217 did not change with sodium selenate treatment in AD or bvFTD.
期刊介绍：
Alzheimer''s & Dementia: Diagnosis, Assessment & Disease Monitoring (DADM) is an open access, peer-reviewed, journal from the Alzheimer''s Association® that will publish new research that reports the discovery, development and validation of instruments, technologies, algorithms, and innovative processes. Papers will cover a range of topics interested in the early and accurate detection of individuals with memory complaints and/or among asymptomatic individuals at elevated risk for various forms of memory disorders. The expectation for published papers will be to translate fundamental knowledge about the neurobiology of the disease into practical reports that describe both the conceptual and methodological aspects of the submitted scientific inquiry. Published topics will explore the development of biomarkers, surrogate markers, and conceptual/methodological challenges. Publication priority will be given to papers that 1) describe putative surrogate markers that accurately track disease progression, 2) biomarkers that fulfill international regulatory requirements, 3) reports from large, well-characterized population-based cohorts that comprise the heterogeneity and diversity of asymptomatic individuals and 4) algorithmic development that considers multi-marker arrays (e.g., integrated-omics, genetics, biofluids, imaging, etc.) and advanced computational analytics and technologies.
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