Evidence map›Paper›PMID 31175982›Full record

ArticleFree radical biology & medicine2019

NEIL1 stimulates neurogenesis and suppresses neuroinflammation after stress.

Beimeng Yang, David M Figueroa, Yujun Hou, Mansi Babbar, Stephanie L Baringer, Deborah L Croteau, Vilhelm A Bohr

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  13. Article
  14. Selective autophagy as a therapeutic target for neurological diseases.Cellular and molecular life sciences : CMLS · 2021
    Review
  15. Neurogenesis After Stroke: A Therapeutic Perspective.Translational stroke research · 2021
    Review
  16. Article
  17. Article
  18. Mitophagy and DNA damage signaling in human aging.Mechanisms of ageing and development · 2020
    Review
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

7 authors at 2 institutions in 2 countries.

Beimeng YangLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
David M FigueroaLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Yujun HouLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Mansi BabbarLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Stephanie L BaringerLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Deborah L CroteauLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
Vilhelm A BohrLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA; Danish Center for Healthy Aging, University of Copenhagen, 2200, Copenhagen, Denmark. Electronic address: vbohr@nih.gov.
National Institutes of Health · USNational Institute on Aging · US

Funding

DNA repair dysfunction in neurodegeneration and Alzheimer's DiseaseZIAAG000723 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT · 2009 to 2025
$9.5M
Oxidative DNA Damage And Its ProcessingZIAAG000727 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2022
$8.4M
OXIDATIVE STRESS MITOCHONDRIAZ01AG000733 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1996 to 2008
$1.6M
Intramural NIH HHS Z01 AG000733
6 · The paper itself

Abstract

Cellular exposure to ionizing radiation leads to oxidatively generated DNA damage, which has been implicated in neurodegenerative diseases. DNA damage is repaired by the evolutionarily conserved base excision repair (BER) system. Exposure of mice to ionizing radiation affects neurogenesis and neuroinflammation. However, the consequences of deficient DNA repair on adult neurogenesis and neuroinflammation are poorly understood despite their potential relevance for homeostasis. We previously reported that loss of NEIL1, an important DNA glycosylase involved in BER, is associated with deficiencies in spatial memory, olfaction, and protection against ischemic stroke in mice. Here, we show that Neil1

Indexed as

Behavior, AnimalInflammationAgingAnimalsApoptosisCell ProliferationCentral Nervous SystemDNA DamageDNA GlycosylasesDNA RepairFearGamma RaysGene Expression ProfilingHippocampusMaleMaze LearningDNA GlycosylasesNeil1 protein, mouseRNADNA damageDNA microarrayNEIL1NeurogenesisNeuroinflammation

Identifiers

PMID31175982
PMCPMC7526462
OpenAlexW2950435398

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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 Socratic graph.