Evidence map›Paper›PMID 38007650›Full record

ArticleJournal of Alzheimer's disease : JAD2023

Clinical Evaluation of Cerebrospinal Fluid p217tau and Neurofilament Light Chain Levels in Patients with Alzheimer's Disease or Other Neurological Diseases.

Takeshi Kawarabayashi, Takumi Nakamura, Kazuya Miyashita, Tatsuya Segawa, Isamu Fukamachi, Takashi Sugawara, Hironori Oka, Kunihiko Ishizawa, Masakuni Amari, Hiroo Kasahara and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-weighted citation impact, top 20% of its field
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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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  3. Early diagnosis of Parkinson's disease: biomarker study.Frontiers in aging neuroscience · 2025
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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

14 authors at 3 institutions in 1 country.

Takeshi KawarabayashiDepartment of Neurology, Dementia Research Center, Geriatrics Research Institute and Hospital, Maebashi, Japan.
Takumi NakamuraDepartment of Neurology, Gunma University Hospital, Maebashi, Japan.
Kazuya MiyashitaImmuno-Biological Laboratories Co., Ltd, Fujioka, Japan.
Tatsuya SegawaImmuno-Biological Laboratories Co., Ltd, Fujioka, Japan.
Isamu FukamachiImmuno-Biological Laboratories Co., Ltd, Fujioka, Japan.
Takashi SugawaraDepartment of Neurology, Dementia Research Center, Geriatrics Research Institute and Hospital, Maebashi, Japan.
Hironori OkaDepartment of Neurology, Dementia Research Center, Geriatrics Research Institute and Hospital, Maebashi, Japan.
Kunihiko IshizawaDepartment of Neurology, Dementia Research Center, Geriatrics Research Institute and Hospital, Maebashi, Japan.
Masakuni AmariDepartment of Neurology, Dementia Research Center, Geriatrics Research Institute and Hospital, Maebashi, Japan.
Hiroo KasaharaDepartment of Neurology, Gunma University Hospital, Maebashi, Japan.
Kouki MakiokaDepartment of Neurology, Gunma University Hospital, Maebashi, Japan.
Yoshio IkedaDepartment of Neurology, Gunma University Hospital, Maebashi, Japan.
Masamitsu TakatamaDepartment of Neurology, Dementia Research Center, Geriatrics Research Institute and Hospital, Maebashi, Japan.
Mikio ShojiDepartment of Neurology, Dementia Research Center, Geriatrics Research Institute and Hospital, Maebashi, Japan.
Gunma University Hospital · JPHirosaki University · JPMedical & Biological Laboratories (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe cerebrospinal fluid (CSF) levels of tau phosphorylated at threonine 217 (p217tau) or 181 (p181tau), and neurofilament light chain (NfL) are definite biomarkers of tauopathy and neurodegeneration in Alzheimer's disease (AD).

objectiveTo validate their utility in excluding other neurological diseases and age-related changes in clinical settings.

methodsWe developed monoclonal antibodies against p217tau and NfL, established novel ELISAs, and analyzed 170 CSF samples from patients with AD or other neurological diseases.

resultsIn AD, p217tau is a more specific and abundant CSF component than p181tau. However, CSF NfL levels increase age-dependently and to a greater extent in central and peripheral nervous diseases than in AD.

conclusionsCSF p217tau correlates better with AD neurodegeneration than other tau-related biomarkers and the major phosphorylated tau species. The clinical usage of NfL as a neurodegeneration biomarker in AD requires exclusion of various central and peripheral neurological diseases.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBiomarkersHumansIntermediate FilamentsNeurofilament Proteinstau ProteinsAmyloid beta-PeptidesBiomarkersMAPT protein, humanneurofilament protein LNeurofilament Proteinstau ProteinsAlzheimer’s diseasecerebrospinal fluidneurofilament light chainneurological diseasesp181taup217tautotal tau

Identifiers

PMID38007650
PMCPMC10741340
OpenAlexW4388967569

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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Registered trials

None linked

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.