Evidence map›Paper›PMID 25448603›Full record

ArticleNeurobiology of aging2015

Loss of NEIL1 causes defects in olfactory function in mice.

Chandrika Canugovi, Magdalena Misiak, Morten Scheibye-Knudsen, Deborah L Croteau, Mark P Mattson, Vilhelm A Bohr

Abstract read
In one paragraph

Article in Neurobiology of aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
0.3field-weighted citation impact, top 47% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Chandrika CanugoviLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Magdalena MisiakLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA; Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Morten Scheibye-KnudsenLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Deborah L CroteauLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Mark P MattsonLaboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Vilhelm A BohrLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA. 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
Cellular And Molecular Pathogenesis Of Alzheimer's DiseaseZIAAG000312 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.4M
GROWTH ARREST AND DNA DAMAGE INDUCIBLE GENE GADD153--REGULATION BY DNA DAMAGEZ01AG000723 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM · 1992 to 2008
$310k
Intramural NIH HHS Z01 AG000723
6 · The paper itself

Abstract

Oxidative DNA damage accumulation has been implicated in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. The base excision repair pathway is a primary responder to oxidative DNA damage. Effects of loss of base excision repair on normal brain function is a relatively nascent area of research that needs further exploration for better understanding of related brain diseases. Recently, we found that loss of a versatile DNA glycosylase endonuclease 8-like 1 (NEIL1) causes deficits in spatial memory retention using the Morris water maze test. Furthermore, we found that there is a significant loss of NEIL1 enzyme levels and its activity in postmortem Alzheimer's disease brains. Based on the Allen Brain Atlas in situ hybridization data, the expression levels of Neil1 messenger RNA are higher in the olfactory bulb compared with other areas of the brain. Olfaction in mice is a central brain function that involves many central nervous system pathways. Here, we studied the effect of complete loss of Neil1 gene on olfactory function. We explored olfactory function in mice with 3 different behavioral tests namely, olfactory sensitivity, performance, and buried food tests. Neil1(-/-) mice performed poorly compared with wild-type mice in all 3 tests. Our data indicate that loss of Neil1 causes olfactory function deficits supporting our previous findings and that normal brain function requires robust DNA repair.

Indexed as

AnimalsDNA DamageDNA GlycosylasesDNA RepairMice, TransgenicOlfaction DisordersOxidative StressSmellDNA GlycosylasesNeil1 protein, mouseAging, smellBase excision repairDNA repairGlycosylaseNEIL1Olfactory senseOxidative DNA damageOxidative stress

Identifiers

PMID25448603
PMCPMC5576891
OpenAlexW1987937561

What OpenQuestion holds

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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 OpenQuestion graph.