ArticleJournal of aging research2011
A novel mouse model of Alzheimer's disease with chronic estrogen deficiency leads to glial cell activation and hypertrophy.
Article in Journal of aging research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Premenstrual dysphoric disorder as a potential predisposing factor for Alzheimer's disease: a review.Frontiers in endocrinology · 2025Review
- Endocrine Dyscrasia in the Etiology and Therapy of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2024Review
- Gender and Neurosteroids: Implications for Brain Function, Neuroplasticity and Rehabilitation.International journal of molecular sciences · 2023Review
- Hippocampal glial inflammatory markers are differentially altered in a novel mouse model of perimenopausal cerebral amyloid angiopathy.Frontiers in aging neuroscience · 2023Article
- Letrozole treatment alters hippocampal gene expression in common marmosets (Callithrix jacchus).Hormones and behavior · 2023Article
- Angiotensin II differentially affects hippocampal glial inflammatory markers in young adult male and female mice.Learning & memory (Cold Spring Harbor, N.Y.) · 2022Article
- Oestrogenic Regulation of Mitochondrial Dynamics.International journal of molecular sciences · 2022Review
- The Impact of Estradiol on Neurogenesis and Cognitive Functions in Alzheimer's Disease.Cellular and molecular neurobiology · 2020Review
- Cognitive Effects of Aromatase and Possible Role in Memory Disorders.Frontiers in endocrinology · 2018Review
- The endocrine dyscrasia that accompanies menopause and andropause induces aberrant cell cycle signaling that triggers re-entry of post-mitotic neurons into the cell cycle, neurodysfunction, neurodegeneration and cognitive disease.Hormones and behavior · 2015Review
- Sex, stroke, and inflammation: the potential for estrogen-mediated immunoprotection in stroke.Hormones and behavior · 2013Review
- Expression of FSH and its co-localization with FSH receptor and GnRH receptor in rat cerebellar cortex.Journal of molecular histology · 2013Article
- Letrozole Potentiates Mitochondrial and Dendritic Spine Impairments Induced by β Amyloid.Journal of aging research · 2013Article
- Mast cell-glia axis in neuroinflammation and therapeutic potential of the anandamide congener palmitoylethanolamide.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2012Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of estrogens in Alzheimer's disease (AD) involving β-amyloid (Aβ) generation and plaque formation was mostly tested in ovariectomized mice with or without APP mutations. The aim of the present study was to explore the abnormalities of neural cells in a novel mouse model of AD with chronic estrogen deficiency. These chimeric mice exhibit a total FSH-R knockout (FORKO) and carry two transgenes, one expressing the β-amyloid precursor protein (APPsw, Swedish mutation) and the other expressing presenilin-1 lacking exon 9 (PS1Δ9). The most prominent changes in the cerebral cortex and hippocampus of these hypoestrogenic mice were marked hypertrophy of both cortical neurons and astrocytes and an increased number of activated microglia. There were no significant differences in the number of Aβ plaques although they appeared less compacted and larger than those in APPsw/PS1Δ9 control mice. Similar glia abnormalities were obtained in wild-type primary cortical neural cultures treated with letrozole, an aromatase inhibitor. The concordance of results from APPsw/PS1Δ9 mice with or without FSH-R deletion and those with letrozole treatment in vitro (with and without Aβ treatment) of primary cortical/hippocampal cultures suggests the usefulness of these models to explore molecular mechanisms involved in microglia and astrocyte activation in hypoestrogenic states in the central nervous system.
Identifiers
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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.