Evidence map›Paper›PMID 37078472›Full record

ArticleAging cell2023

Deletion of quinolinate phosphoribosyltransferase gene accelerates frailty phenotypes and neuromuscular decline with aging in a sex-specific pattern.

Tae Chung, Taylor Bopp, Chris Ward, Francesca M Notarangelo, Robert Schwarcz, Reyhan Westbrook, Qian-Li Xue, Jeremy Walston, Ahmet Hoke

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 36% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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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

9 authors at 2 institutions in 1 country.

Tae ChungDepartment of Physical Medicine and Rehabilitation, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID 0000-0002-0270-5181
Taylor BoppDepartment of Physical Medicine and Rehabilitation, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Chris WardDepartment of Orthopedics, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Francesca M NotarangeloMaryland Psychiatric Research Center, Department of Psychiatry, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Robert SchwarczMaryland Psychiatric Research Center, Department of Psychiatry, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Reyhan WestbrookDepartment of Geriatric Medicine and Gerontology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Qian-Li XueDepartment of Geriatric Medicine and Gerontology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Jeremy WalstonDepartment of Geriatric Medicine and Gerontology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Ahmet HokeDepartment of Neurology, Neuromuscular Division, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Johns Hopkins University · USUniversity of Maryland, Baltimore · US

Funding

Technological Assessment and Solutions Core - RC4P30AG021334 · NIA · JOHNS HOPKINS UNIVERSITY · PI Jeremy D Walston · 2003 to 2026
$33.2M
Alteration of kynurenine pathway in age-associated muscle weaknessK08AG058483 · NIA · JOHNS HOPKINS UNIVERSITY · PI CHUNG, TAE HWAN · 2018 to 2022
$854k
NIA NIH HHS K08 AG058483NIA NIH HHS P30 AG021334
6 · The paper itself

Abstract

Decline in neuromuscular function with aging is known to be a major determinant of disability and all-cause mortality in late life. Despite the importance of the problem, the neurobiology of age-associated muscle weakness is poorly understood. In a previous report, we performed untargeted metabolomics on frail older adults and discovered prominent alteration in the kynurenine pathway, the major route of dietary tryptophan degradation that produces neurotoxic intermediate metabolites. We also showed that neurotoxic kynurenine pathway metabolites are correlated with increased frailty score. For the present study, we sought to further examine the neurobiology of these neurotoxic intermediates by utilizing a mouse model that has a deletion of the quinolinate phosphoribosyltransferase (QPRT) gene, a rate-limiting step of the kynurenine pathway. QPRT

Indexed as

FrailtyKynurenineAgingAnimalsFemaleMaleMiceMuscle WeaknessNicotinate-Nucleotide Diphosphorylase (Carboxylating)PhenotypeKynurenineNicotinate-Nucleotide Diphosphorylase (Carboxylating)age-associated muscle weaknessagingfrailtykynurenineneurodegenerationneuromuscular junctionquinolinic acidsarcopenia

Identifiers

PMID37078472
PMCPMC10352574
OpenAlexW4366463972

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.