Unlocking therapeutic strategies for menopausal cognitive decline


Dive into the research presented by Rhonda R. Voskuhl at ACOG 2024, shedding light on the potential of estrogen receptor beta as a target to mitigate cognitive decline in postmenopausal women.

At the 2024 ACOG Annual Clinical & Scientific Meeting, Rhonda R. Voskuhl, MD, professor of Neurology at the University of California, Los Angeles, presented an oral abstract titled, “Mind the Gap: Estrogen receptor beta in astrocytes is a therapeutic target to prevent cognitive problems at menopause.”

Voskuhl discussed the presentation in an interview with Contemporary OB/GYN. The abstract highlighted the unmet need of psychological decline among postmenopausal women. Estrogens are neuroprotective, making the loss of estrogen during menopause associated with neurodeficiency. However, data about this association remains lacking.

Cognitive domain-specific deficits that may occur in even healthy postmenopausal women include working memory, verbal memory, and processing. Imaging abnormalities will also be observed among women with these deficits.

These issues impair women’s ability to work and interact socially, indicating significant adverse outcomes. In the abstract, investigators conducted a study to identify the cell and brain region mediating these cognitive issues during menopause.

Outcomes were observed in a mouse model, include young, midlife, and senior mice. When estrogen was taken away from young and midlife mice through an oophorectomy, cognitive outcomes were not significantly impacted. However, a significant sex-hormone by age interaction was observed, leading to adverse outcomes among aging midlife and senior mice.

In the older mice, MRI scans showed dorsal hippocampal atrophy alongside cognitive decline. This indicated clinical and pathology deficits following estrogen decline at midlife aging.

The abstract also discussed methods for solving these adverse outcomes. Investigators evaluates the impact of estrogen receptor beta, which is expressed in the brain. Additionally, prior data has indicated neuroprotective effects from estrogen receptor beta compared to estrogen receptor alpha.

Unlike estrogen receptor alpha, estrogen receptor beta is expressed in the brain rather than the breasts, preventing chronic breast stimulation while providing neuroprotection. This optimizes efficacy and reduces toxicity.

In the mice model, loss of estrogen receptor beta in the astrocytes was associated with critical outcomes. However, administration of an estrogen receptor beta ligand and estradiol reversed this pathology and led to improved outcomes.

Finally, Voskuhl mentioned how this treatment can be translated to humans. During RNA-sequencing analysis, glucose utilization was impacted by estrogen receptor beta loss, indicating a lack of simulation in astrocytes. This data can be considered in future treatment.

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