| Paper | Paper Session 08 Program Schedule
02/15/2024
04:00 pm - 05:25 pm
Room: West Side Ballroom - Salon 3
Paper Session 08: Cognitive Aging and Related Topics 2
Final Abstract #3
DNA Methylation Age Acceleration as a Predictor of Midlife Cognitive Status
Sophie Bell, University of Virginia, Charlottesville, United States
Christopher Beam, University of Southern California, Los Angeles, United States
Deborah Finkel, 1. Center for Economic and Social Research, University of Southern California; 2. Institute for Gerontology, Jönköping University, Jönköping, Sweden, Los Angeles, United States
A. Barna, Norton Children’s Research Institute affiliated with the University of Louisville School of Medicine, Louisville, United States
Ariel King, Norton Children’s Research Institute affiliated with the University of Louisville School of Medicine, Louisville, United States
Kendra Sikes, Norton Children’s Research Institute affiliated with the University of Louisville School of Medicine, Louisville, United States
Lesa Ryan, Norton Children’s Research Institute affiliated with the University of Louisville School of Medicine, Louisville, United States
Deborah Davis, Norton Children’s Research Institute affiliated with the University of Louisville School of Medicine, Louisville, United States
Eric Turkheimer, University of Virginia, Charlottesville, United States
Category: Aging
Keyword 1: cognitive functioning
Keyword 2: genetics
Objective:
The epigenome is malleable; early lifestyle and environmental exposures may have lasting effects on rate of aging as indexed by alterations to the epigenome. DNA methylation (DNAm) age measures predict age-related morbidities and mortality better than chronological age. The Louisville Twin Study (LTS), which now comprises a childhood and midlife phase, presents a unique opportunity to clarify the role of early life environmental exposures and cognitive development in biological and cognitive aging at midlife. We expect that DNAm age measures trained to predict age related outcomes and death, independent of chronological age, will be sensitive to cognitive ability in midlife.
Participants and Methods:
Data collection of the midlife phase of the LTS is ongoing. This study presents preliminary results on 254 individual twins, with a mean age of 51.9 years (SD = 7.15). The sample includes 33 DZ and 54 MZ complete twin pairs. Adult cognitive ability was measured using the Wechsler Adult Intelligence Scale Fourth Edition (WAIS-IV). Mean midlife FSIQ is 106.3 (SD = 13.8). DNAm age acceleration was calculated using six clock algorithms, Horvath 1, Horvath 2, Hannum, GrimAge, PhenoAge, and DNAm Telomere Length (DNAmTL). Multiple linear regression models were used to investigate the relationship between DNAm age acceleration and cognitive functioning from childhood to midlife. All models included chronological age, gender, childhood socioeconomic status (SES), and childhood cognitive ability as covariates to account for their influence on adult cognitive ability.
Results:
After controlling for chronological age, childhood cognitive ability, gender, and SES, DNAm GrimAge (b = −0.68, SE = 0.15, p <.001) and PhenoAge (b = −0.24, SE = 0.11, p <.05) remained significantly associated with general cognitive functioning in midlife.
Conclusions:
Our findings suggest that DNAm age acceleration is independently associated with adult IQ scores, even after accounting for SES, childhood IQ, and gender. GrimAge acceleration and PhenoAge acceleration, two second generation DNAm age clocks, are predictive of cognitive aging outcomes, but no causative relationship can be inferred from cross-sectional studies.
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