Epigenetic clocks association with brain aging patterns in older women

Exploratory Score: 0.900 Price: $0.50 cognitive impairment and dementia human patients Status: proposed

What This Experiment Tests

Exploratory experiment designed to discover new patterns targeting N/A in human patients. Primary outcome: Association between epigenetic clocks and brain aging patterns (SPARE-BA and AD-PS)

Description

This longitudinal study examined the associations between five different epigenetic clocks measured at baseline and two brain aging measures derived from structural MRI scans obtained approximately 8 years later. The study focused on 1,196 older women and investigated whether epigenetic age acceleration is associated with brain structural changes indicative of aging and Alzheimer's disease pathology. The epigenetic clocks included various measures of biological age acceleration based on DNA methylation patterns. The brain aging measures included the Spatial Pattern of Atrophy for Recognition of Brain Aging (SPARE-BA), which captures general brain aging patterns, and the Alzheimer's Disease Pattern Similarity Score (AD-PS), which reflects structural changes characteristic of Alzheimer's disease. Linear regression models were used to assess associations while controlling for relevant demographic and health-related covariates. The study found no significant associations between any epigenetic clock and SPARE-BA, but identified a significant positive association between AgeAccelGrim2 and AD-PS.

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TARGET GENE
N/A
MODEL SYSTEM
human patients
ESTIMATED COST
$0
TIMELINE
0 months
PATHWAY
DNA methylation aging pathways
SOURCE
extracted_from_pmid_41949889
PRIMARY OUTCOME
Association between epigenetic clocks and brain aging patterns (SPARE-BA and AD-PS)

Scoring Dimensions

Info Gain 0.00 (25%) Feasibility 0.00 (20%) Hyp Coverage 0.00 (20%) Cost Effect. 0.00 (15%) Novelty 0.00 (10%) Ethical Safety 0.00 (10%) 0.900 composite

📖 Wiki Pages

dna-damage-repairmechanismDNA Damage Repair Mechanisms Across NeurodegeneratmechanismDNA Damage-Accumulating Neurons in NeurodegeneraticellMRI Atrophy Patterns in CBS/PSPbiomarkerMRI and Imaging Findings in Corticobasal SyndromediagnosticDNA Methylation Biomarkers in NeurodegenerationbiomarkerDNA Damage Response in Corticobasal SyndromemechanismDNA MethylationentityDNA Damage Repair Deficiency Validation Study in PexperimentDNA Damage and Repair in NeuronscellDNA Damage Repair Deficiency Hypothesis in ParkinshypothesisDNA Damage Repair Therapy - Biomarker GuidedideaDNA Damage Repair Investment LandscapeinvestmentDNA Damage Response in Alzheimer's DiseasemechanismDNA Damage Response Impairment Pathwaymechanism

Protocol

  • Establish human patients cohorts for cognitive impairment and dementia and predefine inclusion, exclusion, and quality-control criteria before intervention. 2. Apply the experimental manipulation described for the nominated disease mechanism, alongside matched control or comparator arms, and document dose, exposure window, and sample timing in a locked protocol log. 3. Measure Association between epigenetic clocks and brain aging patterns (SPARE-BA and AD-PS) together with orthogonal secondary readouts such as molecular, imaging, behavioral, or safety endpoints that are appropriate to the title and study design. 4.
  • ...

    Expected Outcomes

    Expected to find associations between epigenetic age acceleration and accelerated brain aging patterns, particularly those associated with dementia risk

    Success Criteria

    • Prespecified primary endpoint (Association between epigenetic clocks and brain aging patterns (SPARE-BA and AD-PS)) improves versus control with p < 0.05 or an equivalent corrected threshold used by the study.
    • The effect size is biologically meaningful and reproduced across technical/biological replicates or the validation subset.
    • Safety, data quality, and missingness remain within protocol-defined bounds so the result is interpretable rather than driven by attrition or assay failure.

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