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Viability Assays for Cells in Culture
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Hormesis and brain diseases.

Vernise J T Lim1, Nishat I Tabassum1, Jacqueline M Orian2

  • 1La Trobe Institute for Molecular Science, La Trobe University, Melbourne, VIC, Australia; Department of Microbiology, Anatomy, Physiology and Pharmacology, School of Agriculture, Biomedicine and Environment, La Trobe University, Melbourne, VIC, Australia.

Progress in Brain Research
|August 6, 2025
PubMed
Summary
This summary is machine-generated.

Low-dose stressors, like exercise and fasting, activate beneficial brain repair pathways through neurohormesis, promoting brain health and delaying neurodegeneration in aging. This process enhances cellular resilience against age-related cognitive decline.

Keywords:
AgingEpigeneticsHormesisIntermittent fastingMulti-omicsNeurodegeneration

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Area of Science:

  • Neuroscience
  • Aging Research
  • Cellular Biology

Background:

  • Aging brain faces metabolic, oxidative, and inflammatory challenges contributing to neurodegeneration.
  • Neurohormesis describes neuronal adaptive responses to mild stress, enhancing cellular repair mechanisms.
  • Age-related decline impairs brain's stress response capacity, increasing vulnerability to neurodegenerative diseases.

Purpose of the Study:

  • To explore the role of neurohormesis in brain health and aging.
  • To investigate how low-dose stressors promote adaptive responses and resilience in neurons.
  • To highlight the potential of hormetic interventions in delaying neurodegeneration and cognitive decline.

Main Methods:

  • Review of literature on hormesis and neurohormesis in the context of brain aging.
  • Analysis of molecular pathways activated by stress-resilience mechanisms (e.g., NRF2, CREB, BDNF).
  • Examination of dietary interventions like calorie restriction (CR) and intermittent fasting (IF) and their impact on brain health.

Main Results:

  • Low-dose stressors (exercise, fasting, dietary compounds) activate neuroprotective signaling pathways.
  • Calorie restriction and intermittent fasting stimulate key molecular targets (NRF2, CREB, BDNF) that regulate stress response and cognitive function.
  • Mitochondrial health, autophagy, and circadian rhythms are crucial in aging and are modulated by CR and IF-induced neurohormesis.

Conclusions:

  • Neurohormesis offers promising therapeutic strategies for enhancing brain resilience against age-related cognitive decline.
  • Understanding neurohormesis can lead to targeted interventions to combat neurodegeneration.
  • Advanced technologies like multi-omics and epigenetics can further elucidate hormesis's protective effects on brain health.