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Related Experiment Video

Updated: May 31, 2026

Measuring Frailty in HIV-infected Individuals. Identification of Frail Patients is the First Step to Amelioration and Reversal of Frailty

Measuring Frailty in HIV-infected Individuals. Identification of Frail Patients is the First Step to Amelioration and Reversal of Frailty

Published on: July 24, 2013

Exploring biologically relevant pathways in frailty.

Yen-Yi Ho¹, Amy M Matteini, Brock Beamer

¹Division of Geriatric Medicine and Gerontology, Johns Hopkins University School of Medicine, 5505 Bayview Circle, Baltimore, MD 21224, USA. jwalston@jhmi.edu

The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences

|July 12, 2011

Summary

This summary is machine-generated.

Genetic variations in inflammation and muscle maintenance genes may influence late-life frailty. This study identified specific gene loci strongly associated with frailty, offering insights into its biological pathways.

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Frailty Assessment in an Aging Mouse Model

Frailty Assessment in an Aging Mouse Model

Published on: September 23, 2025

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Last Updated: May 31, 2026

Measuring Frailty in HIV-infected Individuals. Identification of Frail Patients is the First Step to Amelioration and Reversal of Frailty

Measuring Frailty in HIV-infected Individuals. Identification of Frail Patients is the First Step to Amelioration and Reversal of Frailty

Published on: July 24, 2013

Frailty Assessment in an Aging Mouse Model

Frailty Assessment in an Aging Mouse Model

Published on: September 23, 2025

Area of Science:

Gerontology
Genetics
Molecular Biology

Background:

Frailty is a complex late-life syndrome characterized by vulnerability, muscle weakness, fatigue, and inflammation.
Understanding frailty's biological pathways is challenging due to its complexity and overlap with disease states.
Genetic analysis offers a promising approach to uncover biological pathways influencing frailty and longevity.

Purpose of the Study:

To investigate the association between genetic variations in inflammation and muscle maintenance genes and frailty.
To identify specific gene loci that may contribute to the development of frailty.

Main Methods:

Genotyped 1,354 single-nucleotide polymorphisms across 134 candidate genes using Illumina platform.
Employed a cross-sectional study design to determine the association strength between frailty and genotype.
Controlled for family-wise false-discovery rate at 0.05 for statistical significance.

Main Results:

No single-nucleotide polymorphism reached study-wide significance after stringent statistical correction.
Single-nucleotide polymorphisms within the 5-methyltetrahydrofolate-homocysteine methyltransferase (MTR), Caspase 8 (CASP8), CREB-binding protein (CREBBP), lysine acetyltransferase 2B (KAT2B), and beta-transducin repeat containing (BTRC) loci showed strong associations with frailty.
These findings suggest potential roles for these specific genes in frailty pathogenesis.

Conclusions:

Preliminary genetic analysis highlights apoptosis and transcription regulation pathways potentially involved in frailty.
Results align with prior gene expression studies in frail mouse models.
Identified gene loci provide etiological insights for future biological investigations into frailty.