ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2025
Cell Adhesion Molecule Protocadherin-γC5 Ameliorates Aβ Plaque Pathogenesis by Modulating Astrocyte Function in Alzheimer's Disease.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Protocadherin gamma subfamily A, 3 inhibits the proliferation and metastasis of lung adenocarcinoma by inhibiting transforming growth factor β signaling pathway.Respiratory research · 2026Article
- Protocadherin γC4 Promotes Neuronal Survival in the Mouse Retina Through Its Variable Cytoplasmic Domain.Molecular neurobiology · 2025Article
- Astrocytes Lingering at a Crossroads: Neuroprotection and Neurodegeneration in Neurocognitive Dysfunction.International journal of biological sciences · 2025Review
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7 authors.
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Abstract
Accumulation of astrocytes around β-amyloid (Aβ) plaques is one of the earliest neuropathological changes in Alzheimer's disease (AD), but the underlying mechanisms and significance remain unclear. Cell adhesion molecule protocadherin-γC5 (Pcdh-γC5) has been reported to implicate in AD. Here, we find elevated expression levels of Pcdh-γC5 in the brain of 5×FAD mice and Aβ-treated astrocytes and further reveal that Pcdh-γC5 deficiency leads to exacerbated Aβ deposition in 5×FAD mice. Deletion of Pcdh-γC5 impairs astrocyte migration, astrocytic response to Aβ signaling, and Aβ phagocytosis in both cultured astrocytes in vitro and 5×FAD mice in vivo. Both male and female mice were used in this study. Our findings support a model in which increased expression level of Pcdh-γC5 promotes astrocyte migration in response to Aβ signaling and engulfment and phagocytosis of neurotoxic Aβ plaques, therefore exerting a critical neuroprotective function in AD.
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