Evidence map›Paper›PMID 39821479›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025

Plasma N-terminal tau fragment is an amyloid-dependent biomarker in Alzheimer's disease.

Guoyu Lan, Laihong Zhang, Anqi Li, Wenqing Ran, Jieqin Lv, Fernando Gonzalez-Ortiz, Yue Cai, Pan Sun, Lin Liu, Jie Yang and 17 more

Abstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Plasma N-terminal tau fragment is an amyloid-dependent biomarker in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    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.

Guoyu LanInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China.
Laihong ZhangInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China.
Anqi LiInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China.
Wenqing RanDepartment of Nuclear Medicine, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Jieqin LvDepartment of Nuclear Medicine, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China.
Fernando Gonzalez-OrtizInstitute of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden.
Yue CaiInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China.
Pan SunInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China.
Lin LiuInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China.
Jie YangInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China.
Zhengbo HeInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China.
Lili FangInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China.
Xin ZhouInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China.
Yalin ZhuInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China.
Zhen LiuInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China.
Xuhui ChenDepartment of Neurology, Peking University Shenzhen Hospital, Shenzhen, China.
Xiang FanDepartment of Medical Imaging, Peking University Shenzhen Hospital, Shenzhen, China.
Dai ShiNeurology Medicine Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, China.
Chenghui YeNeurology Medicine Center, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, China.
Linsen XuDepartment of Medical Imaging, Shenzhen Guangming District People's Hospital, Shenzhen, China.
Qingyong WangDepartment of Neurology, Shenzhen Guangming District People's Hospital, Shenzhen, China.
Kaj BlennowInstitute of Neuroscience and Physiology, University of Gothenburg, Mölndal, Sweden.
Guanxun ChengDepartment of Medical Imaging, Peking University Shenzhen Hospital, Shenzhen, China.
Alzheimer's Disease Neuroimaging Initiative
Pengcheng RanDepartment of Nuclear Medicine, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China.
Lu WangDepartment of Nuclear Medicine, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Tengfei GuoInstitute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, China.ORCID 0000-0003-2982-0865

Funding

Alzheimer's Disease Neuroimaging Initiative - SupplementU01AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI WEINER, MICHAEL W · 2004 to 2015
$121.0M
Guangdong Basic and Applied Basic Science Foundation for Distinguished Young Scholars 2023B1515020113Lingang Laboratory LG-GG-202401-ADA070600National Key Research and Development Program of China 2023YFC3605400National Natural Science Foundation of China 82171197National Natural Science Foundation of China 82301380NIA NIH HHS U01 AG024904Shenzhen Bay Laboratory S241101004-1Shenzhen Science and Technology Program RCYX20221008092935096
6 · The paper itself

Abstract

introductionNovel fluid biomarkers for tracking neurodegeneration specific to Alzheimer's disease (AD) are greatly needed.

methodsUsing two independent well-characterized cohorts (n = 881 in total), we investigated the group differences in plasma N-terminal tau (NT1-tau) fragments across different AD stages and their association with cross-sectional and longitudinal amyloid beta (Aβ) plaques, tau tangles, brain atrophy, and cognitive decline.

resultsPlasma NT1-tau significantly increased in symptomatic AD and displayed positive associations with Aβ PET (positron emission tomography) and tau PET. Higher baseline NT1-tau levels predicted greater tau PET, with 2- to 10-year intervals and faster longitudinal Aβ PET increases, AD-typical neurodegeneration, and cognitive decline. Plasma NT1-tau showed negative correlations with baseline regional brain volume and thickness, superior to plasma brain-derived tau (BD-tau) and neurofilament light (NfL) in Aβ-positive participants. DISCUSSION: This study suggests that plasma NT1-tau is an Aβ-dependent biomarker and outperforms BD-tau and NfL in detecting cross-sectional neurodegeneration in the AD continuum. HIGHLIGHTS: Plasma N-terminal tau (NT1-tau) was specifically increased in the A+/T+ stage. Plasma NT1-tau was positively associated with greater amyloid beta (Aβ) and tau PET (positron emission tomography) accumulations. Higher plasma NT1-tau predicted greater tau burden and faster Aβ increases. Plasma NT1-tau was more related to neurodegeneration than plasma brain-derived tau (BD-tau) and neurofilament light (NfL).

Indexed as

Alzheimer DiseaseAmyloid beta-Peptidestau ProteinsAgedAged, 80 and overAtrophyBiomarkersBrainCognitive DysfunctionCross-Sectional StudiesFemaleHumansLongitudinal StudiesMaleMiddle AgedPeptide FragmentsAmyloid beta-PeptidesBiomarkersMAPT protein, humanPeptide Fragmentstau ProteinsAlzheimer's diseaseBD‐taucognitive declineneurodegenerationNfLNT1‐tau

Identifiers

PMID39821479
PMCPMC11881634

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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 OpenQuestion graph.