SynthesisThe Cochrane database of systematic reviews2010
Neuroprotection for treatment of glaucoma in adults.
Synthesis in The Cochrane database of systematic reviews, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
16 citing papers in PubMed, 3 syntheses or guidelines pooled it, 29 citations in OpenAlex.
- Neuroprotection for treatment of glaucoma in adults.The Cochrane database of systematic reviews · 2017Pooled it
- Neuroprotection for treatment of glaucoma in adults.The Cochrane database of systematic reviews · 2013Pooled it
- Interventions for age-related visual problems in patients with stroke.The Cochrane database of systematic reviews · 2012Pooled it
- Nanotechnology for Medical and Surgical Glaucoma Therapy-A Review.Advances in therapy · 2020Review
- IL-1 Family Members Mediate Cell Death, Inflammation and Angiogenesis in Retinal Degenerative Diseases.Frontiers in immunology · 2019Review
- Protective effects ofMolecular vision · 2018Article
- Determination of Serum Ceruloplasmin Concentration in Patients with Primary Open Angle Glaucoma with Cataract and Patients with Cataract Only: A Pilot Study.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Long-term assessment of prostaglandin analogs and timolol fixed combinations vs prostaglandin analogs monotherapy.International journal of ophthalmology · 2016Article
- Psychophysical testing in rodent models of glaucomatous optic neuropathy.Experimental eye research · 2015Review
- Current perspective of neuroprotection and glaucoma.Clinical ophthalmology (Auckland, N.Z.) · 2015Review
- Glaucomatous optic neuropathy management: the role of neuroprotective agents.Medical hypothesis, discovery & innovation ophthalmology journal · 2013Review
- A ketogenic diet may offer neuroprotection in glaucoma and mitochondrial diseases of the optic nerve.Medical hypothesis, discovery & innovation ophthalmology journal · 2012Article
- A model for the easy assessment of pressure-dependent damage to retinal ganglion cells using cyan fluorescent protein-expressing transgenic mice.Molecular vision · 2012Article
- Clinical evidence for neuroprotection in glaucoma.American journal of ophthalmology · 2011Article
- Quantification of deficits in spatial visual function of mouse models for glaucoma.Investigative ophthalmology & visual science · 2011Article
- Closed gateways--can neuroprotectants shield the retina in glaucoma?Drugs in R&D · 2010Article
Corrections and comments
- Updated by
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundGlaucoma is a heterogeneous group of conditions involving progressive damage to the optic nerve, deterioration of retinal ganglion cells and ultimately visual field loss. It is a leading cause of blindness worldwide. Open angle glaucoma (OAG), the commonest form of glaucoma, is a chronic condition that may or may not present with increased intraocular pressure (IOP). Neuroprotection for glaucoma refers to any intervention intended to prevent optic nerve damage or cell death. The treatment can target extracellular factors such as reducing IOP, or cellular factors derived from the optic nerve itself such as blocking intracellular death signals.
objectivesThe objective of this review was to systematically examine the evidence regarding the effectiveness of neuroprotective agents, either topical or oral, for slowing the progression of OAG in adults. SEARCH STRATEGY: We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (which contains the Cochrane Eyes and Vision Group Trials Register) (The Cochrane Library, Issue 4, 2009), MEDLINE (January 1960 to January 2010), EMBASE (January 1980 to January 2010), Latin American and Caribbean Literature on Health Sciences (LILACS) (January 1982 to January 2010) and ClinicalTrials.gov (http://clinicaltrials.gov). (5 January 2010). There were no language or date restrictions in the search for trials. The electronic databases were last searched on 5 January 2010. SELECTION CRITERIA: This review was limited to randomized controlled trials (RCTs) in which topical or oral treatments were used to prevent retinal ganglion cell death. Our population of interest was adults with OAG. As the primary outcome for this review was the proportion of participants who developed any progression of visual field loss at five years post intervention, only trials with at least five years of follow-up were included. DATA COLLECTION AND ANALYSIS: Two review authors independently reviewed titles and abstracts from the literature searches. Full text copies of relevant or potentially relevant studies were obtained and re-evaluated for inclusion. There were no trials identified for this review, thus we performed no data extraction or meta-analysis. Two studies comparing memantine to placebo are currently awaiting classification until additional study details are provided. Reasons for excluding studies from the review were documented. MAIN
resultsIn accordance with the selection criteria for inclusion, we identified no studies relevant for this review. The results of short-term trials and other studies are discussed in this review. AUTHORS'
conclusionsAlthough neuroprotective agents are intended to act as pharmacological antagonists to prevent cell death, the evidence that they are effective in preventing retinal ganglion cell death, and thus preserving vision in patients with OAG, has not been demonstrated. Long-term RCTs are needed to determine whether or not neuroprotective agents may be beneficial for individuals with OAG.
Indexed as
Identifiers
What OpenQuestion holds
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.