ArticleLife science alliance2025
Loss of PLA2G4E compromises synaptic structure and cognitive outcomes in mice.
Article in Life science alliance, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Reprogramming lipid metabolism for cognitive restoration in Alzheimer's via PLA2G4E.Alzheimer's & dementia (New York, N. Y.)Article
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Given its potential role in supporting cognitive resilience, PLA2G4E has emerged as a compelling therapeutic target in the context of Alzheimer's disease (AD). However, its physiological functions in the central nervous system remain largely unexplored. In this study, we demonstrate that Pla2g4e expression peaks during early postnatal brain development, coinciding with the rapid formation of synapses. Loss-of-function experiments in primary neuronal cultures revealed that Pla2g4e expression is essential for proper dendritic development and neuronal maturation. In constitutive Pla2g4e knockout mice, we observed significant disruptions in the developmental profiles of cortical synaptic plasticity markers, accompanied by impairments in memory-related behaviors. Notably, the adeno-associated virus-mediated overexpression of
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