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<p>The relationship between epigenetic age acceleration (EAA) and midlife cognitive function remains unclear, with limited causal evidence. We investigated this association in 1252 Black and White middle-aged adults from the Bogalusa Heart Study (BHS) and conducted a two-sample Mendelian randomization (MR) analysis using GWAS summary statistics for EAA (<i>N</i> = 34,710) and cognition (<i>N</i> ≤ 106,162). In BHS, higher Hannum age acceleration, PhenoAge acceleration, and GrimAge acceleration (GrimAA) were each associated with slower processing speed (<i>p</i> &lt; 0.05). Additionally, GrimAA was linked to lower global cognition scores (<i>p</i> &lt; 0.001), independent of covariates. MR analysis suggested a potential link, showing that genetically predicted GrimAA was nominally associated with slower processing speed (<i>p</i> = 0.05). These findings suggest that epigenetic aging, particularly GrimAA, is independently associated with lower cognitive function in midlife and may play an important role in cognitive impairment, especially in processing speed.</p>

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Epigenetic age acceleration and midlife cognition: joint evidence from observational study and Mendelian randomization

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月18日

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  • Yang Pan,
  • Zhijie Huang,
  • Xiao Sun,
  • Ileana De Anda-Duran,
  • Ruiyuan Zhang,
  • Wei Chen,
  • Changwei Li,
  • Ana W. Capuano,
  • Kristine Yaffe,
  • Jinying Zhao,
  • David A. Bennett,
  • Owen T. Carmichael,
  • Lydia A. Bazzano,
  • Tanika N. Kelly

摘要

The relationship between epigenetic age acceleration (EAA) and midlife cognitive function remains unclear, with limited causal evidence. We investigated this association in 1252 Black and White middle-aged adults from the Bogalusa Heart Study (BHS) and conducted a two-sample Mendelian randomization (MR) analysis using GWAS summary statistics for EAA (N = 34,710) and cognition (N ≤ 106,162). In BHS, higher Hannum age acceleration, PhenoAge acceleration, and GrimAge acceleration (GrimAA) were each associated with slower processing speed (p < 0.05). Additionally, GrimAA was linked to lower global cognition scores (p < 0.001), independent of covariates. MR analysis suggested a potential link, showing that genetically predicted GrimAA was nominally associated with slower processing speed (p = 0.05). These findings suggest that epigenetic aging, particularly GrimAA, is independently associated with lower cognitive function in midlife and may play an important role in cognitive impairment, especially in processing speed.