ArticleInternational journal of molecular sciences2020
Neuroprotection of Retinal Ganglion Cells with AAV2-BDNF Pretreatment Restoring Normal TrkB Receptor Protein Levels in Glaucoma.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 54 citations in OpenAlex.
- Aptamers in Ocular Disease Therapy and Drug Delivery: Current Progress and Future Opportunities.Current therapeutic research, clinical and experimental · 2026Review
- Research progress on molecular therapy for glaucoma (Review).Molecular medicine reports · 2026Review
- Experimental models to study oxidative stress in glaucoma: integratingFrontiers in pharmacology · 2026Review
- Article
- Targeted Neuroprotection of Retinal Ganglion Cells Via AAV2-hSyn-NGF Gene Therapy in Glaucoma Models.Investigative ophthalmology & visual science · 2025Article
- Emerging strategies targeting genes and cells in glaucoma.Vision research · 2025Review
- The role of RGC degeneration in the pathogenesis of glaucoma.International journal of biological sciences · 2025Review
- The role of neurotrophic factors in retinal ganglion cell resiliency.Frontiers in cellular neuroscience · 2025Review
- Challenging glaucoma with emerging therapies: an overview of advancements against the silent thief of sight.Frontiers in medicine · 2025Review
- Exploring Glaucoma: From Pathogenesis to Emerging Diagnostic and Management Strategies.Journal of ophthalmology · 2025Review
- Neuritin 1 Drives Therapeutic Preservation of Retinal Ganglion Cells in anJournal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2024Article
- Molecular Mechanisms of Glaucoma Pathogenesis with Implications to Caveolin Adaptor Protein and Caveolin-Shp2 Axis.Aging and disease · 2024Review
- Advances in Neuroprotection in Glaucoma: Pharmacological Strategies and Emerging Technologies.Pharmaceuticals (Basel, Switzerland) · 2024Review
- AAV-mediated gene therapies for glaucoma and uveitis: are we there yet?Expert reviews in molecular medicine · 2024Review
- Molecular pathways in experimental glaucoma models.Frontiers in neuroscience · 2024Review
- The concept of gene therapy for glaucoma: the dream that has not come true yet.Neural regeneration research · 2024Review
- The Neuroprotective Effect of Activation of Sigma-1 Receptor on Neural Injury by Optic Nerve Crush.Investigative ophthalmology & visual science · 2023Article
- Selectively compromised inner retina function following hypoxic-ischemic encephalopathy in mice: A noninvasive measure of severity of the injury.Neurochemistry international · 2023Article
- Use of gene therapy for optic nerve protection: Current concepts.Frontiers in neuroscience · 2023Review
- Secreted phosphoprotein 1 slows neurodegeneration and rescues visual function in mouse models of aging and glaucoma.Cell reports · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Intravitreal delivery of brain-derived neurotrophic factor (BDNF) by injection of recombinant protein or by gene therapy can alleviate retinal ganglion cell (RGC) loss after optic nerve injury (ONI) or laser-induced ocular hypertension (OHT). In models of glaucoma, BDNF therapy can delay or halt RGCs loss, but this protection is time-limited. The decreased efficacy of BDNF supplementation has been in part attributed to BDNF TrkB receptor downregulation. However, whether BDNF overexpression causes TrkB downregulation, impairing long-term BDNF signaling in the retina, has not been conclusively proven. After ONI or OHT, when increased retinal BDNF was detected, a concomitant increase, no change or a decrease in TrkB was reported. We examined quantitatively the retinal concentrations of the TrkB protein in relation to BDNF, in a course of adeno-associated viral vector gene therapy (AAV2-BDNF), using a microbead trabecular occlusion model of glaucoma. We show that unilateral glaucoma, with intraocular pressure ( IOP) increased for five weeks, leads to a bilateral decrease of BDNF in the retina at six weeks, accompanied by up to four-fold TrkB upregulation, while a moderate BDNF overexpression in a glaucomatous eye triggers changes that restore normal TrkB concentrations, driving signaling towards long-term RGCs neuroprotection. We conclude that for glaucoma therapy, the careful selection of the appropriate BDNF concentration is the main factor securing the long-term responsiveness of RGCs and the maintenance of normal TrkB levels.
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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 OpenQuestion graph.