Neuroprotective Frontiers in Glaucoma: Synaptic Stability and Trophic Modulation

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About this Research Topic

Submission deadlines

  1. Manuscript Submission Deadline 29 May 2026

  2. This Research Topic is currently accepting articles.

Background

Glaucoma represents a critical challenge in ocular medicine as one of the leading causes of irreversible blindness. Traditional therapies primarily focus on lowering intraocular pressure (IOP); however, this approach does not completely halt the degeneration of retinal ganglion cells (RGCs), which leads to progressive vision loss. Current research underscores the need for innovative and experimental strategies that preserve synaptic integrity and target underlying pathophysiological mechanisms, such as neurotrophin deprivation and neuroinflammation, to enhance RGC survival. Recent advancements in understanding molecular pathways—such as those involved in glutamate excitotoxicity, mitochondrial dysfunction, and oxidative stress—are pivotal in identifying novel neuroprotective therapies.

This Research Topic aims to consolidate innovative strategies for neuroprotection, especially those applicable to glaucoma, which may also have wider applications across neurodegenerative diseases. By focusing on neurotrophin- and neurotransmitter-based therapies, we seek to highlight groundbreaking approaches that could provide renewed hope for individuals affected worldwide. Progress in neuroprotective strategies is accelerating, with new combinatory approaches like AAV2-mediated BDNF gene therapy and CNTF-secreting implants showing promise by enhancing neuronal resilience and ameliorating traditional challenges like systemic toxicity and blood-retinal barrier permeability.

To gather further insights into the realm of glaucoma neuroprotection, we welcome articles addressing, but not limited to, the following themes:

Neurotrophin engineering strategies utilizing viral vectors and nanoparticle delivery for sustained BDNF/NGF/CNTF release

Synaptic stabilization through ocular-specific NMDA antagonists and GABA-A receptor modulators

AI-driven drug discovery and dual-target ligands like TrkB agonists and glutamate scavengers

Clinical integration of combined therapies merging IOP-lowering agents with neuroprotectives

Proteomic/transcriptomic biomarkers development for personalized approaches in addressing RGC loss

While the thematic focus is on neurotrophic signaling and synaptic homeostasis, this topic also encompasses broader mechanisms like oxidative stress and neuroinflammation contributing to RGC degeneration. We aim to foster a platform that welcomes diverse scientific contributions and encourages interdisciplinary collaboration to push glaucoma management towards more effective neurocentric approaches. Various formats of submission, including original research articles, reviews, and case studies, are welcome to enhance our understanding of this transformative area in glaucoma therapy.

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Article types and fees

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

  • Brief Research Report
  • Data Report
  • Editorial
  • FAIR² Data
  • FAIR² DATA Direct Submission
  • General Commentary
  • Hypothesis and Theory
  • Methods
  • Mini Review

Articles that are accepted for publication by our external editors following rigorous peer review incur a publishing fee charged to Authors, institutions, or funders.

Keywords: Glaucoma, Neuroprotection, Retinal Ganglion Cells, Neurotrophic Signaling, Synaptic Homeostasis, Excitotoxicity, Gene Therapy, Neurotransmitter Modulation, Precision Medicine, Vision Preservation

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Manuscripts can be submitted to this Research Topic via the main journal or any other participating journal.

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