Evidence map›Paper›PMID 38157030›Full record

ArticleJournal of neurology2024

Cerebrospinal fluid NPTX2 changes and relationship with regional brain metabolism metrics across mild cognitive impairment due to Alzheimer's disease.

Federico Massa, Caterina Martinuzzo, Nerea Gómez de San José, Virginia Pelagotti, Wendy Kreshpa, Samir Abu-Rumeileh, Lorenzo Barba, Pietro Mattioli, Beatrice Orso, Andrea Brugnolo and 9 more

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In one paragraph

Article in Journal of neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 15% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Cerebrospinal fluid NPTX2 and [Alzheimer's research & therapy · 2025
    Article
  6. Article
  7. Article
  8. Article
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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

19 authors at 6 institutions in 2 countries.

Federico MassaDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy. fedemassa88@gmail.com.ORCID http://orcid.org/0000-0001-5667-204X
Caterina MartinuzzoDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy.
Nerea Gómez de San JoséDepartment of Neurology, Ulm University Hospital, Ulm, Germany.
Virginia PelagottiDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy.
Wendy KreshpaDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy.
Samir Abu-RumeilehDepartment of Neurology, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany.
Lorenzo BarbaDepartment of Neurology, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany.
Pietro MattioliDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy.
Beatrice OrsoDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy.
Andrea BrugnoloDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy.
Nicola GirtlerDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy.
Tiziana VigoIRCCS Ospedale Policlinico San Martino, Genoa, Italy.
Dario ArnaldiDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy.
Carlo SerratiNeurology Unit, ASL 1 Hospital, Imperia, Italy.
Antonio UccelliDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy.
Silvia MorbelliIRCCS Ospedale Policlinico San Martino, Genoa, Italy.
Andrea ChincariniNational Institute of Nuclear Physics (INFN), Genoa Section, Genoa, Italy.
Markus OttoDepartment of Neurology, Martin-Luther-University Halle-Wittenberg, Halle (Saale), Germany.
Matteo PardiniDepartment of Neuroscience, Rehabilitation, Ophthalmology, Genetics, Maternal and Child Health (DINOGMI), University of Genoa, Genoa, Italy.
Ospedale Policlinico San Martino · ITUniversity of Genoa · ITMartin Luther University Halle-Wittenberg · DEAzienda Sanitaria Locale Roma 3 · ITIstituto Nazionale di Fisica Nucleare · ITUniversity Hospital Ulm · DE

Funding

Ministero dell'Università e della Ricerca PE0000006
6 · The paper itself

Abstract

backgroundNeuronal pentraxin-2 (NPTX2), crucial for synaptic functioning, declines in cerebrospinal fluid (CSF) as cognition deteriorates. The variations of CSF NPTX2 across mild cognitive impairment (MCI) due to Alzheimer's disease (AD) and its association with brain metabolism remain elusive, albeit relevant for patient stratification and pathophysiological insights.

methodsWe retrospectively analyzed 49 MCI-AD patients grouped by time until dementia (EMCI, n = 34 progressing within 2 years; LMCI, n = 15 progressing later/stable at follow-up). We analyzed demographic variables, cognitive status (MMSE score), and CSF NPTX2 levels using a commercial ELISA assay in EMCI, LMCI, and a control group of age-/sex-matched individuals with other non-dementing disorders (OND). Using [

resultsBaseline and follow-up MMSE scores were lower in LMCI than EMCI (p value = 0.006 and p < 0.001). EMCI exhibited significantly higher CSF NPTX2 values than both LMCI (p = 0.028) and OND (p = 0.006). We found a significant positive correlation between NPTX2 values and metabolism of bilateral precuneus in MCI-AD patients (p < 0.005 at voxel level, p < 0.05 with family-wise error correction at the cluster level).

conclusionsHigher CSF NPTX2 in EMCI compared to controls and LMCI suggests compensatory synaptic responses to initial AD pathology. Disease progression sees these mechanisms overwhelmed, lowering CSF NPTX2 approaching dementia. Positive CSF NPTX2 correlation with precuneus glucose metabolism links to AD-related metabolic changes across MCI course. These findings posit CSF NPTX2 as a promising biomarker for both AD staging and progression risk stratification.

Indexed as

Alzheimer DiseaseCognitive DysfunctionAmyloid beta-PeptidesBiomarkersBrainDisease ProgressionHumansRetrospective Studiestau ProteinsAmyloid beta-PeptidesBiomarkerstau Proteins[18F]FDG PETAlzheimer's diseaseCerebrospinal fluid biomarkersMild cognitive impairment (MCI)Neuronal pentraxin-2Synaptic dysfunction

Identifiers

PMID38157030
OpenAlexW4390405863

What OpenQuestion holds

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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.