Evidence map›Paper›PMID 40483474›Full record

ArticleAlzheimer's research & therapy2025

Plasma biomarkers for early detection of alzheimer's disease: a cross-sectional study in a Japanese cohort.

Masahito Kubota, Shogyoku Bun, Keisuke Takahata, Shin Kurose, Yuki Momota, Yu Iwabuchi, Toshiki Tezuka, Hajime Tabuchi, Morinobu Seki, Yasuharu Yamamoto and 15 more

Abstract read
In one paragraph

Article in Alzheimer's research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
–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

16 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  9. Review
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  11. Circulating Biomarkers for the Early Diagnosis of Alzheimer's Disease.International journal of molecular sciences · 2025
    Review
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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

25 authors.

Masahito KubotaDepartment of Neurology, Keio University School of Medicine, Tokyo, Japan.
Shogyoku BunDepartment of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.
Keisuke TakahataDepartment of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.
Shin KuroseDepartment of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.
Yuki MomotaDepartment of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.
Yu IwabuchiDepartment of Radiology, Keio University School of Medicine, Tokyo, Japan.
Toshiki TezukaDepartment of Neurology, Keio University School of Medicine, Tokyo, Japan.
Hajime TabuchiDepartment of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.
Morinobu SekiDepartment of Neurology, Keio University School of Medicine, Tokyo, Japan.
Yasuharu YamamotoDepartment of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.
Ryo ShikimotoDepartment of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.
Yu MimuraDepartment of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.
Takayuki HoshinoDepartment of Neurology, Keio University School of Medicine, Tokyo, Japan.
Sho ShimohamaDepartment of Neurology, Keio University School of Medicine, Tokyo, Japan.
Natsumi SuzukiDepartment of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.
Ayaka MorimotoDepartment of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.
Azusa OosumiDepartment of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.
Yuka HoshinoDepartment of Neurology, Keio University School of Medicine, Tokyo, Japan.
Kenji TaiEisai-Keio Innovation Laboratory for Dementia, DCV Function, DHBL, Eisai Co., Ltd, Shinjuku-ku, Tokyo, 160-8582, Japan.
Hirofumi AoyagiEisai-Keio Innovation Laboratory for Dementia, DCV Function, DHBL, Eisai Co., Ltd, Shinjuku-ku, Tokyo, 160-8582, Japan.
Yoshiaki SatoEisai-Keio Innovation Laboratory for Dementia, DCV Function, DHBL, Eisai Co., Ltd, Shinjuku-ku, Tokyo, 160-8582, Japan.
Junro KuromitsuEisai-Keio Innovation Laboratory for Dementia, DCV Function, DHBL, Eisai Co., Ltd, Shinjuku-ku, Tokyo, 160-8582, Japan.
Jin NakaharaDepartment of Neurology, Keio University School of Medicine, Tokyo, Japan.
Masaru MimuraDepartment of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.
Daisuke ItoDepartment of Neurology, Keio University School of Medicine, Tokyo, Japan. d-ito@jk9.so-net.ne.jp.

Funding

Japan Agency for Medical Research and Development JP17pc0101006
6 · The paper itself

Abstract

backgroundPlasma biomarkers offer a promising alternative to amyloid beta (Aβ) positron emission tomography (PET) or cerebrospinal fluid (CSF) biomarkers for diagnosing Alzheimer's disease (AD). This cross-sectional study assessed the utility of multiple plasma biomarkers for diagnosing and staging AD in a Japanese cohort.

methodsThe assessed plasma biomarkers included Aβ42/40, phosphorylated tau (p-tau181 and p-tau217), glial fibrillary acidic protein (GFAP), and neurofilament light chain (NfL), individually and in combination. Aβ42/40 was measured using the HISCL

resultsSixty-nine HC, 13 preclinical AD, 38 AD-MCI, 44 AD-D, and 79 non-AD CI participants were included. The area under the curves (AUCs) for predicting Aβ PET status were 0.937 (Aβ42/40), 0.926 (p-tau217), and 0.946 (p-tau217/Aβ42); results of pair-wise DeLong tests revealed no significant differences among these three metrics (all p > 0.05). In the cognitively normal group, the AUCs were 0.968 (Aβ42/40), 0.958 (p-tau217), and 0.979 (p-tau217/Aβ42), while in the cognitively impaired group, they were 0.919 (Aβ42/40), 0.893 (p-tau217), and 0.923 (p-tau217/Aβ42). Among HC and AD continuum participants, CL correlations were - 0.74 (Aβ42/40), 0.81 (p-tau217), and 0.83 (p-tau217/Aβ42). In the HC and AD continuum, Aβ42/40 levels showed a bimodal distribution (cutoff = 0.096), with a shift from high to low occurring at 19.3 CL, compared to the PET positivity threshold of 32.9 CL. P-tau217 exhibited a linear increase with disease progression. All biomarkers correlated strongly with logical memory scores.

conclusionsPlasma biomarkers, Aβ42/40 and p-tau217, and particularly their ratio (p-tau217/Aβ42), show strong potential as Aβ PET alternatives for AD diagnosis. HISCL-based plasma Aβ42/40 detects Aβ accumulation earlier than Aβ PET visual reading threshold, underscoring its utility as an early diagnostic marker.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBiomarkersAgedAged, 80 and overCognitive DysfunctionCohort StudiesCross-Sectional StudiesEarly DiagnosisEast Asian PeopleFemaleGlial Fibrillary Acidic ProteinHumansJapanMaleMiddle AgedAmyloid beta-Peptidesamyloid beta-protein (1-42)BiomarkersGlial Fibrillary Acidic Proteinneurofilament protein LNeurofilament ProteinsPeptide Fragmentstau ProteinsAlzheimer’s diseaseAβ42/40CentiloidHISCLPlasma biomarkersp-tau217p-tau217/Aβ42Simoa

Identifiers

PMID40483474
PMCPMC12144780

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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.