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dc.contributor.authorGupta, Ankur
dc.date.accessioned2016-11-02T16:42:44Z
dc.date.available2016-11-02T16:42:44Z
dc.date.issued2013-11
dc.identifier.citationMed Hypotheses. 2013 Nov;81(5):797-802. doi: 10.1016/j.mehy.2013.08.023.language
dc.identifier.urihttp://hdl.handle.net/20.500.12904/892
dc.description.abstractGlaucoma is a disease characterized by progressive optic nerve degeneration and is the leading cause of irreversible blindness worldwide. More than 60 million people globally are affected by glaucoma, of which 8 million people suffer from bilateral blindness, making glaucoma the second leading cause of bilateral blindness worldwide. Current management of glaucoma is aimed at reducing intraocular pressure via a number of different strategies. Current treatments do not attempt to correct the underlying pathology of glaucoma, which is the cell degeneration and ultimate death of retinal ganglion cells, thereby limiting their clinical efficacy. A neuroprotective approach to glaucoma management would address the underlying pathology and would, in theory, be beneficial to all patients regardless of risk and causative factors. Here it is proposed that leptin could be used as a potential neuroprotective agent in the management of glaucoma. Leptin has shown neuroprotective promise in a number of neurodegenerative diseases, and there has been increasing evidence that glaucomatous neurodegeneration is analogous to other neurodegenerative diseases in the central nervous system. Leptin could target retinal ganglion cell death by a number of mechanisms, namely apoptosis, oxidative stress and excitotoxicity reduction. This article presents evidence linking current understanding about leptin's neuroprotective effect and the molecular mechanisms underlying glaucoma.language
dc.language.isoenlanguage
dc.subjectGlaucomalanguage
dc.subjectLeptinlanguage
dc.titleLeptin as a neuroprotective agent in glaucoma.language
dc.typeArticlelanguage


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