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Transcriptomic and metabolomic changes might predict frailty in SAMP8 mice.

Letizia Dacomo1, Pietro La Vitola1, Laura Brunelli2

  • 1Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.

Aging Cell
|July 4, 2024
PubMed
Summary

Frailty, a risk factor for Alzheimer's disease, can be predicted early. Senescence-Accelerated Mouse Prone-8 (SAMP8) mice showed memory deficits and muscle weakness, with distinct genetic and metabolic signatures indicating early frailty.

Keywords:
agingdementiafrailtymotor impairmentneuronal losspredictive biomarkerssenescent SAMP8 mice

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Area of Science:

  • Gerontology
  • Neuroscience
  • Metabolomics

Background:

  • Frailty is a multi-dimensional geriatric syndrome linked to reduced resilience and increased risk of Alzheimer's disease (AD).
  • Frailty is considered a reversible condition, highlighting the need for early biomarkers for timely prediction and prevention.
  • Senescence-Accelerated Mouse Prone-8 (SAMP8) mice serve as a preclinical model for studying frailty and its progression.

Purpose of the Study:

  • To investigate the transcriptional and metabolic changes associated with frailty in SAMP8 mice.
  • To identify early biomarkers for frailty that may predict dementia development.
  • To characterize the cognitive, motor, structural, and neuropathological aspects of frailty in SAMP8 mice at different ages.

Main Methods:

  • Characterization of SAMP8 mice at 2.5, 6, and 9 months of age, assessing cognitive, motor, structural, and neuropathological parameters.
  • Transcriptional analysis of brain tissue to identify genetic signatures.
  • Plasma metabolomic analysis to detect metabolic alterations.

Main Results:

  • SAMP8 mice exhibited memory deficits, muscle weakness, and motor impairment starting at 2.5 months of age.
  • Functional deficits were associated with neurodevelopmental issues, including reduced neuronal density and glial cell loss.
  • Transcriptomics revealed distinct genetic signatures in SAMP8 mice by 6 months, while plasma metabolomics identified lower acylcarnitines and lipids in SAMP8 mice from 2.5 months onwards, correlating with functional and neuropathological findings.

Conclusions:

  • Specific genetic alterations in the brain and metabolic changes in plasma can serve as early indicators of frailty.
  • These findings suggest potential biomarkers for early assessment of frailty, paving the way for clinical investigations into dementia prevention.
  • The study underscores the utility of the SAMP8 mouse model for understanding the pathogenesis of frailty and its link to neurodegenerative diseases.