Evidence map›Paper›PMID 41000823›Full record

ArticlebioRxiv : the preprint server for biology2025

Altered NPTX2 dynamics associated with impaired cognitive aging.

Rebecca P Haberman, Ana Delgado, Meifang Xiao, Ming Teng Koh, Ashley A Becker, Shiyu Ji, Paul F Worley, Michela Gallagher, Audrey Branch

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. 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. Article
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

9 authors.

Rebecca P HabermanDepartment of Psychological and Brain Sciences, Johns Hopkins University, Baltimore, MD, USA.
Ana DelgadoSolomon H. Snyder Department of Neuroscience, Johns Hopkins University, Baltimore, MD, USA.
Meifang XiaoSolomon H. Snyder Department of Neuroscience, Johns Hopkins University, Baltimore, MD, USA.
Ming Teng KohDepartment of Psychological and Brain Sciences, Johns Hopkins University, Baltimore, MD, USA.
Ashley A BeckerDepartment of Psychological and Brain Sciences, Johns Hopkins University, Baltimore, MD, USA.
Shiyu JiSolomon H. Snyder Department of Neuroscience, Johns Hopkins University, Baltimore, MD, USA.
Paul F WorleySolomon H. Snyder Department of Neuroscience, Johns Hopkins University, Baltimore, MD, USA.
Michela GallagherDepartment of Psychological and Brain Sciences, Johns Hopkins University, Baltimore, MD, USA.
Audrey BranchDepartment of Psychological and Brain Sciences, Johns Hopkins University, Baltimore, MD, USA.ORCID 0000-0002-5452-2109

Funding

TRANSCRIPTIONAL MECHANISMS OF HIPPOCAMPAL AGINGP01AG009973 · NIA · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI JAMES J KNIERIM · 1991 to 2026
$52.4M
Research Education ComponentP30AG066507 · NIA · JOHNS HOPKINS UNIVERSITY · PI Corinne Pettigrew · 2020 to 2026
$29.3M
NIA NIH HHS P01 AG009973NIA NIH HHS P30 AG066507
6 · The paper itself

Abstract

Changes in synaptic integrity and neural activity homeostasis are hallmarks of brain aging and are closely tied to cognitive outcomes. Yet, defining their relationship across the continuum from normal aging to neurodegenerative disease has proven challenging. Recent research investigating the dynamic changes of neuronal pentraxin 2 (NPTX2, or Narp, neuronal activity-related pentraxin) in cerebrospinal fluid (CSF) of Alzheimer's disease (AD) subjects supports its promise as a prognostic marker of disease progression, possibly as an expression of synaptic damage related to cognitive impairment. However, studies in human subjects are unable to clearly differentiate age-related and disease-related processes. Here we took advantage of a well-characterized rat model that displays substantial individual differences in hippocampal memory during aging, uncontaminated by slowly progressive, spontaneous neurodegenerative disease. Through this approach, we aimed to interrogate the underlying neural substrates that mediate aging as a uniquely permissive condition and the primary risk for neurodegeneration. We found that successful cognitive aging is associated with an elevation of NPTX2 levels above that found in young or cognitively impaired subjects. Pharmacological engagement of neural activity was sufficient to increase NPTX2 levels in all subjects, but cognitively-impaired aged subjects failed to recruit NPTX2 in response to a hippocampus-dependent memory task. Together the findings demonstrate that changes in NPTX2 are coupled to differential cognitive outcomes of aging, and that successful neurocognitive aging is associated with adaptive upregulation of NPTX2, not simply the persistence of youthful synaptic dynamics.

Indexed as

age related cognitive declineBiological Scienceshippocampal hyperactivityNeuronal pentraxin 2Neuroscience

Identifiers

PMID41000823
PMCPMC12458184

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.