Evidence map›Paper›PMID 40035863›Full record

ArticleCellular and molecular life sciences : CMLS2025

NEIL3 influences adult neurogenesis and behavioral pattern separation via WNT signaling.

Marion S Fernandez-Berrocal, Amilcar Reis, Veslemøy Rolseth, Rajikala Suganthan, Anna Kuśnierczyk, Arthur França, Annara Y M Soares, Nicolas Kunath, Anna M Bugaj, Andreas Abentung and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Exploring the Impact of 3-Pharmaceuticals (Basel, Switzerland) · 2025
    Article
  3. 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

15 authors.

Marion S Fernandez-BerrocalDepartment of Clinical and Molecular Medicine (IKOM), Norwegian University of Science and Technology (NTNU), 7491, Trondheim, Norway.
Amilcar ReisDepartment of Neuroscience, Uppsala University, 752 36, Uppsala, Sweden.
Veslemøy RolsethDepartment of Microbiology, Oslo University Hospital, University of Oslo, 0424, Oslo, Norway.
Rajikala SuganthanDepartment of Microbiology, Oslo University Hospital, University of Oslo, 0424, Oslo, Norway.
Anna KuśnierczykDepartment of Clinical and Molecular Medicine (IKOM), Norwegian University of Science and Technology (NTNU), 7491, Trondheim, Norway.
Arthur FrançaNeurodynamics Lab, Brain Institute, Federal University of Rio Grande Do Norte, Natal, 59056-450, Brazil.
Annara Y M SoaresNeurodynamics Lab, Brain Institute, Federal University of Rio Grande Do Norte, Natal, 59056-450, Brazil.
Nicolas KunathDepartment of Clinical and Molecular Medicine (IKOM), Norwegian University of Science and Technology (NTNU), 7491, Trondheim, Norway.
Anna M BugajDepartment of Clinical and Molecular Medicine (IKOM), Norwegian University of Science and Technology (NTNU), 7491, Trondheim, Norway.
Andreas AbentungDepartment of Clinical and Molecular Medicine (IKOM), Norwegian University of Science and Technology (NTNU), 7491, Trondheim, Norway.
Lars EideDepartment of Medical Biochemistry, University of Oslo, Oslo, Norway.
Richardson N LeãoNeurodynamics Lab, Brain Institute, Federal University of Rio Grande Do Norte, Natal, 59056-450, Brazil.
Magnar BjøråsDepartment of Clinical and Molecular Medicine (IKOM), Norwegian University of Science and Technology (NTNU), 7491, Trondheim, Norway. magnar.bjoras@ntnu.no.
Katja SchefflerDepartment of Neuromedicine and Movement Science, Norwegian University of Science and Technology (NTNU), 7491, Trondheim, Norway. katja.scheffler@ntnu.no.
Jing YeDepartment of Clinical and Molecular Medicine (IKOM), Norwegian University of Science and Technology (NTNU), 7491, Trondheim, Norway. jing.ye@ntnu.no.ORCID http://orcid.org/0000-0002-6364-4124

Funding

Norges Forskningsråd 275777Norges Forskningsråd 287911Norges Forskningsråd 297037Norges Forskningsråd 326101
6 · The paper itself

Abstract

Adult neurogenesis in the hippocampus, involving the generation and integration of new neurons, is essential for behavioral pattern separation, which supports accurate memory recall and cognitive plasticity. Here, we explore the role of the DNA repair protein NEIL3 in adult hippocampal neurogenesis and behavioral pattern separation. NEIL3 is required for efficient proliferation and neuronal differentiation of neonatal NSPCs and adult-born NPCs in the hippocampus following a behavioral pattern separation task. NEIL3-depleted mice exhibited a reduced preference for the novel object location, indicating a deficit in pattern separation. NEIL3-deficient adult-born neurons exhibited a significant reduction in mature-like membrane properties, indicating impaired functional maturation. Interestingly, these impairments were not associated with the decreased genomic integrity but with the altered transcriptional regulation of the Wnt signaling pathway. Given the importance of adult neurogenesis in cognitive function, targeting NEIL3 could offer therapeutic potential for addressing age-related hippocampal dysfunction and cognitive decline.

Indexed as

DNA GlycosylasesNeurogenesisWnt Signaling PathwayAnimalsBehavior, AnimalCell DifferentiationCell ProliferationHippocampusMaleMiceMice, Inbred C57BLNeural Stem CellsNeuronsDNA GlycosylasesHippocampal transcriptomeNEIL3 DNA glycosylaseNeural stem and progenitor cells (NSPCs)Novel object location (NOL)Oxidative DNA damagePatch-clamp recording

Identifiers

PMID40035863
PMCPMC11880487

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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.