Evidence map›Paper›PMID 41667480›Full record

Articlenpj aging2026

Frailty phenotype reveals heterogeneity in aging and distinct taurine associations.

April Kim, Rebecca Keener, Ashton Omdahl, Michael Bene, Reyhan Westbrook, Anne Le, Cissy Zhang, Pratik Khare, Mohammed Khadeer, Luigi Ferrucci and 3 more

Abstract read
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In one paragraph

Article in npj aging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

April KimDepartment of Computer Science, Johns Hopkins University, Baltimore, MD, USA.
Rebecca KeenerDepartment of Biomedical Engineering, Johns Hopkins University, Baltimore, MD, USA.
Ashton OmdahlDepartment of Biomedical Engineering, Johns Hopkins University, Baltimore, MD, USA.
Michael BeneDivision of Geriatrics and Gerontology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Reyhan WestbrookDivision of Geriatrics and Gerontology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Anne LeGigantest Inc., Baltimore, MD, USA.
Cissy ZhangGigantest Inc., Baltimore, MD, USA.
Pratik KhareGigantest Inc., Baltimore, MD, USA.
Mohammed KhadeerNational Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Luigi FerrucciNational Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Ruin MoaddelNational Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Alexis BattleDepartment of Computer Science, Johns Hopkins University, Baltimore, MD, USA. ajbattle@jhu.edu.
Peter AbadirDivision of Geriatrics and Gerontology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. pabadir1@jhmi.edu.

Funding

Technological Assessment and Solutions Core - RC4P30AG021334 · NIA · JOHNS HOPKINS UNIVERSITY · PI Jeremy D Walston · 2003 to 2026
$33.2M
NIA NIH HHS P30 AG021334
6 · The paper itself

Abstract

Frailty, characterized by diminished physiological reserve and increased vulnerability to stressors, is a common geriatric syndrome associated with adverse health outcomes. While recent seminal studies have reported conflicting findings regarding taurine, a sulfur-containing amino acid with antioxidant properties, and its relationship with aging, these discrepancies may reflect the heterogeneity of aging trajectories among older adults that chronological age alone fails to capture. Here, we propose that frailty status may better capture this heterogeneity and reveal associations between taurine and aging that are obscured when using age alone. We examined taurine and upstream metabolites in the taurine biosynthesis pathway in 146 community-dwelling adults aged 20-97 years, focusing on older adults (≥69 years) stratified by frailty phenotype. We observed a non-monotonic relationship where taurine levels were highest in robust individuals, lowest in prefrail, and intermediate in frail groups. Analysis of the taurine biosynthesis pathway revealed distinct metabolic profiles across frailty states. Robust individuals demonstrated efficient pathway flux, while the prefrail group exhibited maximal metabolic disruption characterized by bottlenecks. Frail individuals showed persistent metabolic disruption but partial taurine restoration, suggesting compensatory mechanisms. Inflammatory marker associations varied by frailty status, with TNF-α showing a significant negative correlation with taurine specifically in prefrail individuals. These findings demonstrate that frailty status reveals distinct shifts in taurine metabolism and immunological regulation not captured by chronological age alone, providing a more biologically meaningful framework for understanding taurine biology in aging populations.

Identifiers

PMID41667480
PMCPMC13002985

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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.