Evidence map›Paper›PMID 41505233›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2026

Plasma levels of an N-terminal tau fragment predict Alzheimer's and neurodegenerative disease biomarkers in autosomal dominant Alzheimer's disease.

Stephanie A Schultz, Yiwen Rao, Lei Liu, Beth Ostaszewski, Amirah K Anderson, Wai-Ying Wendy Yau, Zahra Shirzadi, Brian A Gordon, Jason Hassenstab, John C Morris and 17 more

Abstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

27 authors.

Stephanie A SchultzDepartment of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA.
Yiwen RaoDepartment of Neurology, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Lei LiuDepartment of Neurology, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Beth OstaszewskiDepartment of Neurology, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Amirah K AndersonDepartment of Neurology, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Wai-Ying Wendy YauDepartment of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA.
Zahra ShirzadiDepartment of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA.
Brian A GordonWashington University in St. Louis School of Medicine, St. Louis, Missouri, USA.
Jason HassenstabWashington University in St. Louis School of Medicine, St. Louis, Missouri, USA.
John C MorrisWashington University in St. Louis School of Medicine, St. Louis, Missouri, USA.
Richard J PerrinWashington University in St. Louis School of Medicine, St. Louis, Missouri, USA.
Ricardo F AllegriDepartment of Cognitive Neurology, Neuropsychiatry and Neuropsychology, Instituto Neurológico Fleni, Buenos Aires, Argentina.
Nicolas R BarthélemyWashington University in St. Louis School of Medicine, St. Louis, Missouri, USA.
Nick FoxDementia Research Centre & UK Dementia Research Institute, UCL Institute of Neurology, London, UK.
Gregory S DayDepartment of Neurology, Mayo Clinic, Jacksonville, Florida, USA.
Mathias JuckerDepartment of Cellular Neurology, German Center for Neurodegenerative Diseases, Tübingen, Germany.
Allan I LeveyDepartment of Neurology, Emory, Atlanta, Georgia, USA.
Johannes LevinDepartment of Clinical Research, German Center for Neurodegenerative Diseases, Munich, Germany.
Hiroshi MoriDepartment of Clinical Neuroscience, Osaka Metropolitan University Medical School, Nagaoka Sutoku University, Osaka, Japan.
Stephen SallowayDepartment of Neurology, Butler Hospital, Providence, Rhode Island, USA.
Peter SchofieldDeparment of Medicine & Health, University of New South Wales, Sydney, Australia.
Eric McDadeWashington University in St. Louis School of Medicine, St. Louis, Missouri, USA.
Reisa A SperlingDepartment of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA.
Randall J BatemanWashington University in St. Louis School of Medicine, St. Louis, Missouri, USA.
Dennis J SelkoeDepartment of Neurology, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Jasmeer P ChhatwalDepartment of Neurology, Massachusetts General Hospital, Boston, Massachusetts, USA.
and the Dominantly Inherited Alzheimer's Network

Funding

Imaging CoreU19AG032438 · NIA · WASHINGTON UNIVERSITY · PI BATEMAN, RANDALL J · 2010 to 2025
$53.9M
Leveraging Heterogeneity in Autosomal Dominant AD to Elucidate Pathophysiology and Improve AD BiomarkersRF1AG079569 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI CHHATWAL, JASMEER P, LIU, LEI · 2022 to 2022
$4.4M
Linking Sleep Disruption to Tau Accumulation and Network Dysregulation in Early Alzheimer's DiseaseR01AG062667 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI CHHATWAL, JASMEER P · 2019 to 2024
$4.2M
Plasma tau and neurodegenerative markers as predictors of rate of AD progressionR01AG071865 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI CHHATWAL, JASMEER P · 2021 to 2025
$4.2M
Leveraging Heterogeneity in Autosomal Dominant AD to Elucidate Pathophysiology and Improve AD BiomarkersR01AG079569 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI JASMEER P CHHATWAL, Michael S Wolfe · 2025 to 2026
$2.8M
Identifying variations in gamma-secretase function that are critical determinants of clinical and biomarker progression of Autosomal Dominant Alzheimer's disease: From mechanism to clinical trialsK01AG084816 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI Stephanie Schultz · 2024 to 2026
$387k
Alzheimer's Association SG-20-690363-DIANDavis APP programInstituto de Salud Carlos IIIJapan Agency for Medical Research and Development JP22dk0207049Japan Agency for Medical Research and Development JP23dk0207066Korea Dementia Research CenterKorea Health Industry Development InstituteMinistry of Health & Welfare and Ministry of Science and ICT, Republic of Korea HI21C0066National Institute on Aging (NIA), the Alzheimer's Association SG-20-690363-DIANNIA NIH HHS K01 AG084816NIA NIH HHS R01 AG062667NIA NIH HHS R01 AG071865NIA NIH HHS R01AG071865NIA NIH HHS R01 AG079569NIA NIH HHS RF1 AG079569NIA NIH HHS U19 AG032438Raul Carrea Institute for Neurological ResearchThe Dominantly Inherited Alzheimer Network U19AG032438
6 · The paper itself

Abstract

introductionTau species lacking truncation of the N-terminal region, including plasma N-terminal tau fragment 1 (NT1), have been previously associated with cognitive decline, neurodegeneration, and tau pathology in late-onset sporadic Alzheimer's disease (AD).

methodsHere, we examined cross-sectional and longitudinal plasma NT1 as a possible predictor of cognitive, clinical, and core AD biomarker trajectories in autosomal dominant AD (ADAD).

resultsNT1 levels in ADAD mutation carriers (MC; n = 132) increased across the disease continuum, compared to non-carriers (NC; n = 75), becoming elevated about a decade prior to estimated symptom onset. Cross-sectional and longitudinal NT1 levels in MC were associated with clinical, cognitive, and biomarker changes. NT1 increases continued in symptomatic phases of disease, a distinct trajectory from that seen with CSF p-tau217 and other phospho-tau species. DISCUSSION: Together, our results suggest that plasma NT1-alone or combined with other tau measures-may be useful in studying AD-related clinical, cognitive, and biomarker outcomes. HIGHLIGHTS: Leveraging a deeply phenotyped cohort of individuals carrying a pathogenic variant for autosomal dominant Alzheimer's disease (ADAD) and their non-carrier family members, our results suggest that plasma N-terminal tau fragment 1 (NT1) levels mirrored changes in clinical, cognitive, and neurodegenerative measures in ADAD, particularly in late asymptomatic and early symptomatic phases of disease. NT1 levels correlated with cerebrospinal fluid (CSF) measures of tau pathology but less so with CSF or imaging measures of β-amyloid pathology. Together with previous supportive findings in preclinical and symptomatic sporadic AD, these results suggest that plasma NT1-alone or combined with other tau measures-may be useful in studying AD-related tau pathology and neurodegeneration across a wide spectrum of disease.

Indexed as

Alzheimer DiseaseNeurodegenerative Diseasestau ProteinsAgedBiomarkersCross-Sectional StudiesFemaleHumansLongitudinal StudiesMaleMiddle AgedMutationPeptide FragmentsBiomarkersPeptide Fragmentstau ProteinsADADbiomarkerneurodegenerationtauopathy

Identifiers

PMID41505233
PMCPMC12782147

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.