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Accelerated epigenetic aging in alcohol dependence.

Toshiyuki Shirai1, Satoshi Okazaki1, Ikuo Otsuka1

  • 1Department of Psychiatry, Kobe University Graduate School of Medicine, Kobe, Japan.

Journal of Psychiatric Research
|March 28, 2024
PubMed
Summary

Alcohol dependence accelerates epigenetic aging, particularly DunedinPACE. Treatment improved GrimAge and GrimAge2 epigenetic clocks, alongside reduced beta-2-microglobulin and Cystatin C levels.

Keywords:
AgingAlcohol dependenceDNA methylationEpigenetic clock

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Area of Science:

  • Epigenetics
  • Aging Research
  • Alcohol Dependence

Background:

  • Alcohol dependence is a global health issue linked to premature aging and mortality.
  • Epigenetic clocks, including GrimAge and DunedinPACE, offer novel insights into biological aging.
  • No prior studies have examined these specific epigenetic markers in alcohol dependence.

Purpose of the Study:

  • To investigate epigenetic age acceleration in alcohol-dependent patients compared to controls.
  • To analyze DNA methylation-based age-predictive components in alcohol dependence.
  • To evaluate the impact of treatment on epigenetic aging markers.

Main Methods:

  • Utilized publicly available DNA methylation data (GSE98876).
  • Analyzed epigenetic clocks: GrimAge, GrimAge2, and DunedinPACE.
  • Compared epigenetic markers before and after a treatment program in patients.

Main Results:

  • DunedinPACE showed accelerated aging in alcohol-dependent patients.
  • AgeAccelGrim and AgeAccelGrim2 decelerated post-treatment.
  • Beta-2-microglobulin and Cystatin C levels decreased after treatment.

Conclusions:

  • Epigenetic aging is altered in alcohol dependence.
  • Treatment may reverse some aspects of epigenetic aging.
  • Findings suggest links to cognitive and psychiatric symptoms.