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Menopause01:28

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Menopause, a natural biological process marking the end of a woman's fertility, typically occurs between the fifth and sixth decade of life. This phase is characterized by the exhaustion of the ovarian follicle pool, leading to less responsive ovaries despite the high levels of Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH). The consequential decrease in estrogen production results in symptoms like hot flashes, heavy sweating, headaches, hair loss, muscle pains, vaginal...
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The ovarian cycle regulates endometrial changes throughout a single menstrual cycle via the coordinated action of gonadotrophin-releasing hormone (GnRH) and gonadotrophins.
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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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The ovarian cycle is meticulously regulated by the hypothalamic-pituitary-gonadal axis. This cycle orchestrates the release of a mature oocyte, essential for reproduction.
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Hormones regulate a significant portion of digestion through activation of the neuroendocrine system. The neuroendocrine system of digestion contains many different hormones all with multiple functions that are both, directly and indirectly, involved in digestion.
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APOE4 Accelerates Menopause-Associated Brain Metabolic Shift and Disrupts Bioenergetic Adaptation.

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The APOE4 gene accelerates menopause-related metabolic decline in the brain, increasing Alzheimer

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Area of Science:

  • Neuroscience and Metabolism
  • Genetics of Alzheimer's Disease

Background:

  • Disrupted brain glucose and lipid metabolism are early indicators of Alzheimer's disease (AD).
  • Menopause-associated estrogen decline elevates AD risk in women by impairing mitochondrial function and glucose metabolism.
  • The APOE4 allele is the strongest genetic risk factor for late-onset AD, further increasing women's risk.

Purpose of the Study:

  • To investigate how APOE genotype influences the menopausal metabolic transition.
  • To examine brain metabolomic and lipidomic changes during peri-to postmenopausal transition in female mice with different APOE genotypes.

Main Methods:

  • Brain metabolomic and lipidomic profiling was performed on female humanized APOE3/3, APOE3/4, and APOE4/4 mice.
  • Mice were studied across chronological and endocrinological stages of the menopausal transition.

Main Results:

  • APOE3/3 mice showed adaptive metabolic regulation supporting postmenopausal energy demands.
  • APOE3/4 and APOE4/4 mice exhibited accelerated, altered metabolic shifts, including amino acid depletion, reduced TCA cycle intermediates, and lipid accumulation.
  • A single APOE4 allele impaired metabolic adaptation; APOE4 homozygosity led to more severe deficits.

Conclusions:

  • APOE4 accelerates menopause-related metabolic decline and impairs brain bioenergetic adaptation.
  • These findings provide a mechanistic link between APOE4, menopausal metabolic changes, and increased susceptibility to Alzheimer's disease in women.