Menopause marks the end of a woman's reproductive years but also the beginning of significant changes in the brain, which may lead to cognitive decline and increase the risk of Alzheimer's disease (AD). Notably, more than two-thirds of all Alzheimer's patients are postmenopausal women, indicating a sex-dependent pathology. Nevertheless, menopause affects over 1 million American women each year. Throughout menopause, estrogen and progesterone production decreases significantly, and menstruation ceases. Recent studies have shown that both hormones result in neuroprotective effects that may explain the heightened risk of AD in postmenopausal women. Addressing the relationship between progesterone and estrogen and their impact on Alzheimer's disease can inform proper treatments to prevent cognitive decline in postmenopausal women.
The findings of "Influence of the Onset of Menopause on the Risk of Developing Alzheimer's Disease" (2024), Dr. Gabriela Briceno Silver and her colleagues delve into the link between menopause and Alzheimer's Disease. AD pathology is currently understood to be caused by amyloid-beta (Aβ) plaques and protein Tau, which damage neurons and result in severe memory impairments. Estrogen prevents the formation of Aβ peptides by modulating the synthesis of amyloid precursor protein (APP). Without estrogen, Aβ peptide production increases and accumulates in the brain to form plaques (Silver et al). Because women have such low levels of estrogen in menopause and postmenopause, these pathways shed light on the susceptibility of women to developing AD.
In the research paper titled "Brain-derived neurotrophic factor and related mechanisms that mediate and influence progesterone-induced neuroprotection" (2024), Dr. Singh et al. studied how progesterone can prevent and treat neurodegenerative diseases such as Alzheimer's and ischemic strokes. Progesterone modulates neurotrophins such as BDNF (brain-derived neurotrophic factor), which promotes neuronal survival, synaptic plasticity, and cognition. It helps to maintain LTP3 by regulating the phosphorylation of NMDA receptors, thus proving its role in memory and cognition.
Dr. Singh mentions hormone replacement therapy (HRT) as a possible treatment for menopausal side effects but underscores the importance of the timing and specific hormone administered. Synthetic progesterone, specifically MPA (Medroxyprogesterone Acetate), suppresses BDNF, preventing neuroprotective effects. Many synthetic progesterones currently used in HRT differ from endogenous progesterone and may not provide the same benefits. Further research is crucial to develop effective HRT protocols to support brain health in postmenopausal women.
The link between menopause and Alzheimer's disease requires scientists to research the phenomena in-depth. Both progesterone and estrogen are crucial for supporting brain processes, although they work in different ways. In addition, it is important to note the biological differences in women. One protocol will not treat all women, and this emphasizes the importance of creating multiple, diverse treatment plans. Exploring these breakthroughs will improve Alzheimer’s disease outcomes and better the quality of life for postmenopausal women.
Briceno Silva, Gabriela, et al. “Influence of the Onset of Menopause on the Risk of Developing Alzheimer’s Disease.” Cureus, vol. 16, no. 9, p. e69124. PubMed Central, https://doi.org/10.7759/cureus.69124.
Singh, Meharvan, et al. “Brain-Derived Neurotrophic Factor and Related Mechanisms That Mediate and Influence Progesterone-Induced Neuroprotection.” Frontiers in Endocrinology, vol. 15, Feb. 2024. Frontiers, https://doi.org/10.3389/fendo.2024.1286066.
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