ArticleResearch square2025
Experimental menopause in 3xTg-AD mice exacerbates metabolic, inflammatory, and osteologic phenotypes aligned with Alzheimer's disease pathology.
Article in Research square, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Peripheral and Central miRNA Signatures in Alzheimer's Disease: Tissue-Specific Variability, Sex-Associated Differences, and Implications for Blood-Based Biomarkers.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Background: Alzheimer's disease (AD) is neurodegenerative disease characterized by the accumulation of amyloid-beta plaques and phosphorylated tau. An estimated 7.2 million Americans are currently living with AD, nearly two-thirds of which are women. Sex differences in AD prevalence and pathology are well established, however the mechanisms underlying these differences are understudied. There are compelling links between menopause and AD, but few established common molecular mechanisms partly due to the lack of representative experimental models. Methods and results: Here, we induce an accelerated ovarian failure (OF) model of menopause in the triple-transgenic AD (3xTg-AD) mouse, using ovotoxin 4-vinylcyclohexene diepoxide (VCD) mediated follicular depletion, leading to a loss of circulating progesterone and an increase in plasma follicle-stimulating hormone (FSH) levels-hormonal changes that closely mirror those observed in human menopause. OF exacerbated peripheral phenotypes associated with AD, namely insulin resistance, inflammation, and bone mass and architecture modifications resembling osteoporosis. OF aggravated age-related impaired glucose tolerance and caused insulin resistance. Additionally, plasma levels of four proinflammatory cytokines- IL-5, IL-6, TNF-α, and CXCL- were all increased in OF mice compared to non-menopausal AD mice. Meanwhile, OF mice display heightened bone loss phenotype, a condition with known links to AD risk and pathology. Conclusion: In summary, accelerated ovarian failure presents key metabolic, inflammatory, and skeletal phenotypes associated with AD, indicating that it can be useful for the identification of novel therapeutic targets.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.