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Basic Science and Pathogenesis.

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Estrogen dominance during perimenopause increases dementia risk by disrupting neuronal cholesterol balance and energy production. This research uncovers a key mechanism linking hormonal changes to Alzheimer's disease susceptibility in aging women.

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Area of Science:

  • Neuroendocrinology
  • Metabolomics
  • Neurodegenerative Diseases

Background:

  • Sex differences in Alzheimer's Disease (AD) are known, but underlying mechanisms involving hormonal interplay are unclear.
  • The perimenopausal transition is linked to cognitive decline and increased dementia risk in women.
  • Cellular changes contributing to this heightened vulnerability in postmenopausal women remain elusive.

Purpose of the Study:

  • To investigate the molecular mechanisms linking hormonal changes during perimenopause to increased Alzheimer's Disease (AD) risk.
  • To explore the role of estrogen and progesterone in neuronal function and energy metabolism.
  • To identify cellular pathways affected by estrogen dominance in the aging female brain.

Main Methods:

  • Analysis of human brain transcriptomic and metabolomic data from the ROSMAP cohort.
  • In vivo studies using mouse models: accelerated ovarian failure, ERRα knockout, and Lafala-AD transgenic models.
  • Behavioral, transcriptomic, metabolomic, and electrophysiological assessments in mouse models.

Main Results:

  • Elevated estradiol to progesterone ratio (estrogen dominance) correlates with cognitive and memory decline.
  • Impaired function of estrogen-related receptor alpha (ERRα) was identified in human brain data.
  • Estrogen dominance disrupts neuronal cholesterol homeostasis, impairs TCA cycle, increases glutamate release, and reduces ATP, heightening susceptibility to AD-related insults.

Conclusions:

  • A novel link between cholesterol balance, mitochondrial energy production, and neuronal function is revealed.
  • Estrogen dominance during perimenopause contributes to increased susceptibility to AD and AD-related dementias in aging women.
  • Findings highlight potential therapeutic targets related to hormonal regulation and metabolic pathways in AD prevention.