ArticleResearch square2026
GPER in murine astrocytes and mural cells promotes neurovascular coupling and Aβ clearance.
Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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Authors and funding
7 authors.
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Abstract
Alzheimer's disease (AD) affects aged women more than men. The precipitous drop in sex hormone levels in postmenopausal women likely contributes to such sexual dimorphism, with emerging evidence implicating the G protein-coupled estrogen receptor (GPER) as a modulator of AD pathology and cognitive impairments. However, the underlying mechanism remains unknown. GPER is distinctively expressed in key components of the neurovascular unit (NVU), namely astrocytes and mural cells (specifically, pericytes). Using GPER-knockout (GPER-KO) and APP/PS1 transgenic AD mouse models, here we show that GPER deficiency exacerbates Aβ deposition, impairs spatial and working memory, and disrupts neurovascular coupling. GPER activation in pericytes reinforces
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