Abstract
Background: Glaucoma is a chronic, vision-threatening disease, and a major cause of legal blindness. The current view is no longer limited to the progressive optic nerve injury, since growing evidence strongly support the interpretation of glaucoma as a complex neurodegenerative disease. However, the precise pathogenic mechanisms leading to the onset and progression of central nervous system (CNS) impairment, and the functional consequences of this damage, are still partially understood. The main aim of this review is to provide a complete and updated overview of the current knowledge regarding the CNS involvement in glaucoma, and the possible therapeutic perspectives.Methods: We made a careful survey of the current literature reporting all the relevant findings related to the cognitive dysfunctions occurring in glaucoma, with specific remarks dedicated on the higher-order visual function impairment and the possible employment of neuroprotective agents.Results: The current literature strongly support the interpretation of glaucoma as a multifaceted chronic neurodegenerative disease, widely affecting the CNS. The cognitive impairment may vary in terms of higher-order functions involvement and in the severity of the degeneration. Although several neuroprotective agents are currently available, the development of new molecules represents a major topic of investigation for future clinical trials.Conclusions: Glaucoma earned the right to be fully considered a neurodegenerative disease. Glaucomatous patients may experience a heterogeneous set of visual and cognitive symptoms, progressively deteriorating the quality of life. Neuroprotection is nowadays a necessary therapeutic goal and a future promising way to preserve visual and cognitive functions, thus improving patients’ quality of life.
Highlights
The term ‘‘glaucoma’’ refers to a group of optic neuropathies characterized by degeneration of retinal ganglion cells (RGCs) and their axons
According to the mechanical theory of glaucoma, Ocular hypertension (OHT) is the result of a backward displacement of the lamina cribrosa, which in turn would damage the axons of RGCs, compressing them between its meshes
Normal tension glaucoma (NTG), which afflicts approximately 15–25% of glaucomatous patients, is a clinical condition in which, despite pathologic cupping of the optic nerve head (ONH) and characteristic visual field (VF) alterations, IOP is within the normal range (Collaborative Normal-Tension Glaucoma Study Group, 1998; Kim and Park, 2016; Mallick et al, 2016)
Summary
The term ‘‘glaucoma’’ refers to a group of optic neuropathies characterized by degeneration of retinal ganglion cells (RGCs) and their axons. To explain NTG-related damages, various non-IOP dependent pathogenetic mechanisms have been proposed, like chronic hypoxia and ischemia, increased intracranial pressure, neuronal glutamate-induced excitotoxicity, mitochondrial dysfunction, oxidative stress, and autoimmunity (Hayreh, 1985; Flammer, 1994; Morgan et al, 1995, 1998, 2002; Romano et al, 1995, 1999; Dreyer et al, 1996; Tezel et al, 1998, 1999; Osborne et al, 2001; Flammer et al, 2002; Gherghel et al, 2005; Grieshaber and Flammer, 2005; Abu-Amero et al, 2006; Grus et al, 2006; Salt and Cordeiro, 2006; Ju et al, 2007; Berdahl et al, 2008a,b; Ren et al, 2010, 2011; Jonas, 2011; Chrysostomou et al, 2013; Siaudvytyte et al, 2014, 2015) Taking together all these factors, a more comprehensive view of glaucoma should be considered, assuming neurodegeneration as a key component of glaucoma pathogenesis. The main aim of this review is to provide a complete and updated overview of the current knowledge regarding the CNS involvement in glaucoma, and the possible therapeutic perspectives
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