Evidence map›Paper›PMID 41787516›Full record

ArticleFluids and barriers of the CNS2026

Plasma p-Tau217 and amyloid-β oligomers as complementary biomarkers for differential diagnosis, comorbidity detection and disease monitoring in idiopathic normal pressure hydrocephalus.

Ko Horikoshi, Madoka Nakajima, Masakazu Miyajima, Ryo Miyahara, Koichiro Sakamoto, Kaito Kawamura, Chihiro Akiba, Chihiro Kamohara, Ikuko Ogino, Taiji Tsunemi and 2 more

Abstract read
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Article in Fluids and barriers of the CNS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

12 authors.

Ko HorikoshiDepartment of Neurosurgery, Juntendo University School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. k-horikoshi@juntendo.ac.jp.
Madoka NakajimaDepartment of Neurosurgery, Juntendo University School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Masakazu MiyajimaDepartment of Neurosurgery, Juntendo University School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Ryo MiyaharaDepartment of Neurosurgery, Juntendo University School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Koichiro SakamotoDepartment of Neurosurgery, Juntendo University School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Kaito KawamuraDepartment of Neurosurgery, Juntendo University School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Chihiro AkibaDepartment of Neurosurgery, Juntendo University School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Chihiro KamoharaDepartment of Neurosurgery, Juntendo University School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Ikuko OginoDepartment of Neurosurgery, Juntendo University School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Taiji TsunemiDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Kostadin KaragiozovDepartment of Neurosurgery, Juntendo University School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Akihide KondoDepartment of Neurosurgery, Juntendo University School of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.

Funding

Japan Society for the Promotion of Science under Grants-in-Aid for Scientific Research 20K09355, 20K09398, and 24K10497Juntendo Research Branding Project, Health, Labor and Welfare Sciences Research Grants 22GB1002
6 · The paper itself

Abstract

backgroundIdiopathic normal pressure hydrocephalus (iNPH) overlaps clinically and pathologically with Alzheimer’s disease (AD), making differential diagnosis and prognostication challenging. The identification of reliable and minimally invasive plasma biomarkers would have major clinical implications for distinguishing iNPH from AD and for monitoring disease course and surgical outcomes.

methodsWe conducted three studies: (Study 1) cross‑sectional comparisons of plasma phosphorylated tau 217 (p‑Tau217) and amyloid-β oligomers (AβO) among healthy controls (HCs; n = 22), iNPH (n = 76), and AD (n = 23) groups, accompanied by receiver operating characteristic (ROC) analysis; (Study 2) correlation analyses within preoperative iNPH group to assess associations between biomarkers and clinical indices, as well as two‑group comparisons between iNPH group with and without AD pathology stratified by CSF p‑Tau181 > 30 pg/mL; and (Study 3) longitudinal pre- and postoperative assessments following shunt surgery.

resultsIn the three‑group analyses, plasma p‑Tau217 effectively discriminated iNPH from AD (AUC = 0.79, 95% = CI 0.700–0.882), whereas discrimination between HCs and iNPH was poor (AUC = 0.48). Plasma AβO moderately discriminated HCs from iNPH (AUC = 0.71, 95% CI = 0.567–0.848). In the preoperative iNPH group, CSF and plasma p‑Tau217 showed a strong correlation (ρ = 0.736, p < 0.001), whereas CSF and plasma AβO showed no significant correlation (ρ = −0.047, p = 0.689). Among iNPH group with AD pathology (CSF p-Tau181 > 30 pg/mL), plasma p-Tau217 was higher, plasma AβO was lower, and Frontal Assessment Battery (FAB) scores were reduced compared with those without AD pathology. For detecting coexistent AD pathology in iNPH group, AUCs were modest for plasma p‑Tau217 (0.64), AβO (0.63), and p‑Tau217/AβO ratio (0.66). Postoperatively, iNPH grading scale (GS), Mini-Mental State Examination (MMSE), and FAB scores improved significantly; CSF and plasma AβO levels decreased, CSF p‑Tau217 increased, whereas plasma p‑Tau217 levels remained stable.

conclusionsPlasma p-Tau217, reflecting AD-related pathology, and plasm AβO, reflecting disease stage, provide complementary information for distinguishing iNPH from AD, assessing comorbidity of AD pathology in iNPH and evaluating postoperative changes. Their combined measurement may support differential diagnosis, aid the preoperative identification of concomitant AD pathology in iNPH, and serve as a minimally invasive screening and triage tool as well as a means of postoperative monitoring, while acknowledging that discrimination between HCs and iNPH at individual level remains limited.

trial registrationNot applicable.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesHydrocephalus, Normal Pressuretau ProteinsAgedAged, 80 and overBiomarkersCross-Sectional StudiesDiagnosis, DifferentialFemaleHumansMalePeptide FragmentsPhosphorylationAmyloid beta-PeptidesBiomarkersMAPT protein, humanPeptide Fragmentstau ProteinsAlzheimer’s diseaseAβOBiomarkerCSFIdiopathic normal pressure hydrocephalusPlasmap-Tau

Identifiers

PMID41787516
PMCPMC13077803

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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.