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Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
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Related Experiment Video

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Sex Stratified Neuronal Cultures to Study Ischemic Cell Death Pathways
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Sex, senescence, senolytics, and cognition.

Thomas C Foster1,2, Ashok Kumar1

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Frontiers in Aging Neuroscience
|March 19, 2025
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Cellular senescence contributes to brain aging and cognitive decline, with sex differences influencing disease risk. Senolytic treatments show potential but interact with sex hormones like estrogen, impacting efficacy.

Keywords:
agingcellular senescencesenolytic treatmentsex differencessex hormone

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Area of Science:

  • Gerontology
  • Neuroscience
  • Cell Biology

Background:

  • Cellular senescence, a state of irreversible cell cycle arrest, is a hallmark of aging, driven by stressors like DNA damage and oxidative stress.
  • Senescent cells release pro-inflammatory cytokines, contributing to systemic inflammation and neuroinflammation, which impairs neuronal function and promotes cognitive decline.
  • Sexual dimorphism exists in aging processes and age-related diseases, potentially linked to sex differences in cell senescence and inflammation.

Purpose of the Study:

  • To review the role of sexual dimorphism in cellular senescence and its impact on brain health and age-related cognitive decline.
  • To explore the efficacy and sex-specific responses to senolytic treatments targeting senescent cells.
  • To understand the interplay between sex hormones, particularly estrogen, and cellular senescence in the aging brain.

Main Methods:

  • Literature review synthesizing current research on cellular senescence, neuroinflammation, cognitive decline, and sex differences.
  • Analysis of studies investigating senolytic interventions in the context of aging and sex.
  • Examination of the molecular mechanisms underlying sex-specific responses to senescence and senolytics.

Main Results:

  • Senescent cells contribute to neuroinflammation and altered neuronal physiology, leading to cognitive decline, with sex differences observed in senescence patterns.
  • Senolytic therapies can ameliorate age-related functional decline by removing senescent cells, but responses vary between males and females.
  • Estrogen influences senescence pathways and has independent anti-aging effects on neurophysiology, interacting with senolytic drug mechanisms.

Conclusions:

  • Sexual dimorphism in cellular senescence and inflammation significantly impacts brain aging and cognitive function.
  • Senolytic treatments offer therapeutic potential for age-related cognitive decline, but their efficacy is modulated by sex and hormonal status.
  • Understanding the complex interplay between sex hormones, senescence, and neurobiology is crucial for developing effective, sex-specific anti-aging strategies.