ArticleScientific reports2025
Retinal degeneration driven by brain-derived neurotrophic factor deficiency in microglia and T-lymphocytes.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Dual immune armies in glaucoma: microglia and monocyte-derived macrophages.Frontiers in immunology · 2026Review
Corrections and comments
- Retracted
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurodegenerative diseases, such as glaucoma or multiple sclerosis, are characterized by progressive neuronal loss involving diverse pathogenic mechanisms. The brain-derived neurotrophic factor (BDNF) has been implicated in neuroprotection and neural plasticity, yet its regulation and involvement in retinal neurodegenerative diseases remain largely unclear. In this study, we investigated the impact of BDNF deficiency in immune cells on retinal integrity. Using mice with a conditional BDNF knockout in microglia/macrophages and T-cells or selectively in microglia/macrophages, we analyzed retinal changes at 3 and 7 months of age, with wildtype mice as controls. BDNF-deficient mice exhibited early and progressive degeneration of retinal ganglion cells and photoreceptors, accompanied by pronounced astrogliosis, which was exacerbated in aged animals. In 7-month-old mice, adaptive changes in synapses could be documented, evidenced through enhanced expression of the vesicular acetylcholine transporter. These findings demonstrate that BDNF from immune cells plays a crucial role in maintaining retinal homeostasis and that its loss promotes retinal neurodegeneration. Targeting immune cell-derived BDNF may offer novel therapeutic strategies for retinal involvement in neurodegenerative diseases with implications for treatment of glaucoma or multiple sclerosis.
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