ArticleNature communications2023
FSH and ApoE4 contribute to Alzheimer's disease-like pathogenesis via C/EBPβ/δ-secretase in female mice.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- C/EBPβ: A transcription factor associated with the irreversible progression of Alzheimer's disease.CNS neuroscience & therapeutics · 2024Pooled it
- Effects ofFoods (Basel, Switzerland) · 2026Article
- Is Follicle-Stimulating Hormone (FSH) Misnamed? Rethinking Its Role in Menopause as a Systemic Regulator of Bone, Brain, Metabolism, and Aging.Journal of clinical medicine · 2026Review
- The extragonadal biology of gonadotropin hormones: should we rename these?Endocrine connections · 2026Article
- Age at menopause,Research square · 2026Article
- Distinct factors drive the progression of tau pathology in Alzheimer's disease.Fundamental research · 2026Review
- Plasma proteomics link menopause timing to brain aging and dementia risk.Research square · 2026Article
- Fshr gene depletion prevents recognition memory loss, fat accrual and bone loss in Alzheimer's mice.Molecular psychiatry · 2026Article
- Neuron-Enriched Extracellular Vesicle MicroRNAs Reflect Hormone-Sensitive Neural Pathway Changes from Early to Late Perimenopause.medRxiv : the preprint server for health sciences · 2026Article
- Plasma proteomics link menopause timing to brain aging and dementia risk.medRxiv : the preprint server for health sciences · 2026Article
- FSH Signaling in Osteoporosis and Alzheimer's Disease.Current osteoporosis reports · 2026Review
- A preliminary investigation of gene expression and levels of FSH, IL-10, and TNF-α and histological staining in natural aging mice.Turkish journal of obstetrics and gynecology · 2026Article
- Gonadotropins Across the Lifespan: Their role in the Neurodevelopment-Neurodegeneration Continuum.The Yale journal of biology and medicine · 2026Review
- Estropausal gut microbiota transplant improves measures of ovarian function in adult mice.Nature aging · 2026Article
- Microglial serine racemase knockout alleviates Alzheimer-like neuropathology and behavioral deficit via lactylation-mediated anti-inflammation.Communications biology · 2026Article
- Follicle-Stimulating Hormone and Its Emerging Role in Coronary Atherosclerosis Among Postmenopausal Women: A Comprehensive Review.International journal of women's health · 2026Review
- The APOE4-estrogen-microglia axis in perimenopausal cognitive changes: mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Targeting FSH for osteoporosis, obesity, and Alzheimer's disease.Trends in molecular medicine · 2025Review
- The Hypothalamic-Pituitary-Ovarian Axis, Ovarian Disorders, and Brain Aging.Endocrinology · 2025Review
- Clinical Significance of APOE4 Genotyping: Potential for Personalized Therapy and Early Diagnosis of Alzheimer's Disease.Journal of clinical medicine · 2025Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) is the most common dementia. It is known that women with one ApoE4 allele display greater risk and earlier onset of AD compared with men. In mice, we previously showed that follicle-stimulating hormone (FSH), a gonadotropin that rises in post-menopausal females, activates its receptor FSHR in the hippocampus, to drive AD-like pathology and cognitive impairment. Here we show in mice that ApoE4 and FSH jointly trigger AD-like pathogenesis by activating C/EBPβ/δ-secretase signaling. ApoE4 and FSH additively activate C/EBPβ/δ-secretase pathway that mediates APP and Tau proteolytic fragmentation, stimulating Aβ and neurofibrillary tangles. Ovariectomy-provoked AD-like pathologies and cognitive defects in female ApoE4-TR mice are ameliorated by anti-FSH antibody treatment. FSH administration facilitates AD-like pathologies in both young male and female ApoE4-TR mice. Furthermore, FSH stimulates AD-like pathologies and cognitive defects in ApoE4-TR mice, but not ApoE3-TR mice. Our findings suggest that in mice, augmented FSH in females with ApoE4 but not ApoE3 genotype increases vulnerability to AD-like process by activating C/EBPβ/δ-secretase signalling.
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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.