ArticleiScience2025
Microglia target synaptic sites early during excitatory circuit disassembly in neurodegeneration.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Antiepileptic and antiepileptogenic effects ofIBRO neuroscience reports · 2026Article
- Microglia extract neuronal proteolytic organelles via skoupocytosis.bioRxiv : the preprint server for biology · 2026Article
- Dysfunction of α2δ4 leads to photoreceptor degeneration through disrupted synaptic mitochondria and calcium crosstalk.Cell death & disease · 2026Article
- Synaptic control of retinal ganglion cell survival and axon regeneration.Molecular neurodegeneration · 2026Review
- Microglial regulation of synaptic plasticity in transsynaptic degeneration of glaucoma.Frontiers in neuroscience · 2026Review
- An Ex Vivo Explant Model for Studying Glial Interactions in the Mouse Retina.Journal of visualized experiments : JoVE · 2025Article
- Article
- Intermittent fasting reduces glaucomatous damage in an HSP27 autoimmune mouse model.Frontiers in cellular neuroscience · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
During development, microglia prune excess synapses to refine neuronal circuits. In neurodegeneration, understanding the role of microglia-mediated synaptic pruning in circuit remodeling and dysfunction is important for developing therapies aimed at modulating microglial function. Here, we analyzed microglia-mediated synapse disassembly of degenerating postsynaptic neurons in the inner retina. After inducing transient intraocular pressure elevation to injure retinal ganglion cells, microglia increase in number, shift to hyper-ramified morphology, and exhibit greater process movement. Furthermore, due to the greater number of microglia, there is increased colocalization of microglia with synaptic components throughout the inner plexiform layer and with excitatory synaptic sites along individual ganglion cell dendrites. Microglia depletion partially protects ganglion cell function, suggesting that microglia activation may be neurotoxic in early neurodegeneration. Our results demonstrate the important role of microglia in synapse disassembly in degenerating circuits, highlighting that microgliosis is the primary mechanism for increased synapse colocalization early after neuronal injury.
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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 Socratic graph.