Evidence map›Paper›PMID 42326467›Full record

ArticleAlzheimer's & dementia (Amsterdam, Netherlands)

Cerebrospinal fluid NPTX2/p-tau ratio as a biomarker for cognitive decline in neurodegenerative diseases.

Bárbara Fernandes Gomes, Mathias Sauer, Laia Montoliu-Gaya, Maria Franquesa-Mullerat, Alexandre Bejanin, Daniel Alcolea, Alberto Lleó, Ignacio Illán-Gala, Juan Fortea, Kaj Blennow and 4 more

Abstract read
In one paragraph

Article in Alzheimer's & dementia (Amsterdam, Netherlands). 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. Menopausal insomnia as a modifiable node of dementia risk: Mechanistic insights and intervention strategies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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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.

Bárbara Fernandes GomesDepartment of Psychiatry and Neurochemistry Institute of Neuroscience and Physiology The Sahlgrenska Academy at the University of Gothenburg Mölndal Sweden.ORCID https://orcid.org/0000-0002-1512-6699
Mathias SauerDepartment of Psychiatry and Neurochemistry Institute of Neuroscience and Physiology The Sahlgrenska Academy at the University of Gothenburg Mölndal Sweden.
Laia Montoliu-GayaDepartment of Psychiatry and Neurochemistry Institute of Neuroscience and Physiology The Sahlgrenska Academy at the University of Gothenburg Mölndal Sweden.
Maria Franquesa-MulleratSant Pau Memory Unit, IR SANT PAU Hospital de la Santa Creu i Sant Pau Barcelona Spain.
Alexandre BejaninSant Pau Memory Unit, IR SANT PAU Hospital de la Santa Creu i Sant Pau Barcelona Spain.
Daniel AlcoleaSant Pau Memory Unit, IR SANT PAU Hospital de la Santa Creu i Sant Pau Barcelona Spain.
Alberto LleóSant Pau Memory Unit, IR SANT PAU Hospital de la Santa Creu i Sant Pau Barcelona Spain.
Ignacio Illán-GalaSant Pau Memory Unit, IR SANT PAU Hospital de la Santa Creu i Sant Pau Barcelona Spain.
Juan ForteaSant Pau Memory Unit, IR SANT PAU Hospital de la Santa Creu i Sant Pau Barcelona Spain.
Kaj BlennowDepartment of Psychiatry and Neurochemistry Institute of Neuroscience and Physiology The Sahlgrenska Academy at the University of Gothenburg Mölndal Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry Institute of Neuroscience and Physiology The Sahlgrenska Academy at the University of Gothenburg Mölndal Sweden.
Johanna NilssonDepartment of Psychiatry and Neurochemistry Institute of Neuroscience and Physiology The Sahlgrenska Academy at the University of Gothenburg Mölndal Sweden.
Olivia BelbinSant Pau Memory Unit, IR SANT PAU Hospital de la Santa Creu i Sant Pau Barcelona Spain.
Nicholas J AshtonDepartment of Psychiatry and Neurochemistry Institute of Neuroscience and Physiology The Sahlgrenska Academy at the University of Gothenburg Mölndal Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionNeuronal pentraxin 2 (NPTX2) and its use as a ratio with other synaptic proteins has emerged as a prognostic cerebrospinal fluid (CSF) biomarker across neurodegenerative diseases.

methodsUsing a single molecule array (Simoa) method, CSF NPTX2 was measured in 688 individuals from the Sant Pau Initiative on Neurodegeneration, including Alzheimer's disease (AD), dementia with Lewy bodies (DLB), frontotemporal lobar degeneration-related disorders (FTLDrs), and cognitively unimpaired (CU) participants. NPTX2/phosphorylated-tau (p-tau)181 performance was compared to standalone NPTX2 and p-tau181.

resultsThe NPTX2/p-tau ratio enhanced diagnostic performance of standalone NPTX2 and p-tau, particularly for DLB and FTLDrs (area under the curve [AUC] DISCUSSION: NPTX2/p-tau may improve prognostic assessments in patients with cognitive impairment, outperforming standalone biomarkers.

Indexed as

Alzheimer's diseasecerebrospinal fluidcognitive declinedementia with Lewy bodiesfrontotemporal lobar degenerationneuronal pentraxin 2phosphorylated tausingle molecule arraysynaptic protein ratio

Identifiers

PMID42326467
PMCPMC13279535

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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.