On correlative and causal links of replicative epimutations

Zhou, Wanding; Reizel, Yitzhak

doi:10.1016/j.tig.2024.08.008

Trends in Genetics

2024

DOI: 10.1016/j.tig.2024.08.008

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On correlative and causal links of replicative epimutations

Wanding Zhou,

Yitzhak Reizel

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2024

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Cited by 2 publications

References 190 publications

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Rewilding alters mouse epigenetic aging

Zipple,

Zhao,

Kuo

et al. 2024

Preprint

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The aging of mammalian epigenomes fundamentally alters cellular functions, and such changes are the focus of many healthspan and lifespan studies. However, studies of this process typically use mouse models living under standardized laboratory conditions and neglect the impact of variation in social, physical, microbial, and other aspects of the living environment on age-related changes. We examined differences in age-associated methylation changes between traditionally lab-reared and "rewilded" C57BL6/J mice, which lived in an outdoor field environment with enhanced ecological realism. Systematic analysis of age-associated methylation dynamics in the liver indicates a genomic region-conditioned, faster epigenetic aging rate in mice living in the field than those living in the lab, implicating perturbed 3D genome conformation and liver function. Altered epigenetic aging rates were more pronounced in sites that gain methylation with age, including sites enriched for transcription factor binding related to DNA repair. These observations underscore the overlooked role of the social and physical environment in epigenetic aging with implications for both basic and applied aging research.

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Rewilding alters mouse epigenetic aging

Zipple,

Zhao,

Kuo

et al. 2024

Preprint

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Epigenetic signatures of regional tau pathology and cognition in the aging and pathological brain

Goldberg,

Wadhwani,

Dehghani

et al. 2024

Preprint

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Primary age-related tauopathy (PART) and Alzheimer's disease (AD) share hippocampal phospho-tau (p-tau) pathology but differ in p-tau extent and amyloid presence. As a result, PART uniquely enables investigation of amyloid-independent p-tau mechanisms during brain aging. We conducted the first epigenome-wide association (EWAS) study of PART, which yielded 13 new and robust p-tau/methylation associations. We then jointly analyzed PART and AD epigenomes to develop 'TauAge', novel epigenetic clocks that predict p-tau severity in region-specific, age-, and amyloid-independent manners. Integrative transcriptomic analyses revealed that genes involved in synaptic transmission are related to hippocampal p-tau severity in both PART and AD, while neuroinflammatory genes are related to frontal cortex p-tau severity in AD only. Further, a machine learning classifier based on PART-vs-AD epigenetic differences discriminates neuropathological diagnoses and stratifies indeterminate cases into subgroups with disparity in cognitive impairment. Together, these findings demonstrate the brain epigenome's substantial role in linking tau pathology to cognitive outcomes in aging and AD.

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On correlative and causal links of replicative epimutations

Cited by 2 publications

References 190 publications

Rewilding alters mouse epigenetic aging

Rewilding alters mouse epigenetic aging

Epigenetic signatures of regional tau pathology and cognition in the aging and pathological brain

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