ArticleExperimental eye research2025
SPG302 protects retinal ganglion cells and preserves visual function by preserving synaptic activity in a mouse model of glaucoma.
Article in Experimental eye research, 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.
- Synaptic control of retinal ganglion cell survival and axon regeneration.Molecular neurodegeneration · 2026Review
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10 authors.
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Abstract
Glaucoma, a leading cause of irreversible vision loss worldwide, is an optic neuropathy characterized by optic nerve degeneration and retinal ganglion cell (RGC) death. Early glaucomatous damage is often associated with dendritic and synaptic abnormalities in RGCs, yet the mechanisms linking these synaptic alterations to RGC death remain unclear. In a mouse model of glaucoma, treatment with the clinical-stage, synaptogenic small molecule SPG302, a pegylated benzothiazole derivative, demonstrated neuroprotective effects, protecting RGCs and their axons in the glaucomatous retina and also improving retinal function as assessed by pattern electroretinogram testing. Elevated intraocular pressure disrupted synapses, as evidenced by reduced synaptophysin expression and homeostatic increases in Bassoon and PSD95 levels in the inner plexiform layer. SPG302 treatment effectively preserved synaptic integrity by reversing these changes. These findings highlight the therapeutic potential of SPG302 for protecting RGCs and preserving vision by modulating synaptic activity in glaucomatous neurodegeneration.
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