Review of glaucoma management without reported intervention details or outcomes

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Frontiers in Medicine Published May 28, 2026 Medically reviewed May 28, 2026 DOI ↗ By Dr. Ji-eun Park, MD · Brain, Mind & Pain

Key Takeaway

Note that this review lacks reported intervention details or outcomes for glaucoma.

This publication is a narrative review focused on the topic of glaucoma. The scope of the article is broad but lacks specific details regarding the population, setting, or intervention exposure. No sample size or follow-up duration is reported in the source text.

The authors synthesize the topic qualitatively rather than providing quantitative data. There are no reported primary outcomes, secondary outcomes, or adverse events. Consequently, no specific numerical results or effect sizes are available for interpretation.

The review acknowledges significant gaps in the provided data. Limitations include the lack of reported funding, conflicts of interest, and specific study constraints. The certainty of any conclusions is limited by the absence of reported primary results and safety data.

Practice relevance cannot be determined from this source. Clinicians should interpret the qualitative arguments with caution given the missing quantitative evidence and unreported safety profiles.

Study Details

Study typeSystematic review

EvidenceLevel 1

PublishedMay 2026

View Original Abstract ↓

Glaucoma is a heterogeneous group of irreversible and blinding optic neuropathies caused by multiple factors. It is clinically characterized by progressive loss of visual field and decline in visual acuity, ultimately culminating in complete blindness. Hallmark pathological features include progressive degeneration of retinal ganglion cells and atrophy of the optic nerve. Importantly, the pathological process of glaucoma extends far beyond the eyeball, involving transsynaptic degeneration across the entire visual pathway. Microglia, as the principal immune regulators of the central nervous system, serve as the earliest sensors and effectors in the pathogenesis of glaucoma. By modulating synaptic plasticity, microglia contribute to synaptic loss and the disruption of neural circuits. They also play essential roles in maintaining neural tissue homeostasis. This review summarizes current evidence and underlying mechanisms of bidirectional transsynaptic degeneration in glaucoma. It highlights that targeting microglial functional homeostasis, particularly their regulation of synaptic plasticity, may be a promising strategy to mitigate glaucoma-associated transsynaptic degeneration and promote central neuroprotection.