Coma, retinal ailments, retinal ganglion cells, endocannabinoids, phytocannabinoids. 1. INTRODUCTION: GLAUCOMA AND RETINAL NEURODEGENERATION Glaucoma comprises a group of eye issues that will cause progressive and/or irreversible blindness. It impacts the elderly but is becoming far more widespread also amongst younger people today and also youngsters [1, 2]. Glaucoma is typically caused by improved intraocular pressure (IOP), even though other variables are involved like progressive harm of retinal ganglion cells (RGCs), referred to as “the messengers of retina”, top to optic nerve degeneration [35]. These situations lead to distinct visual field defects, and at some point total vision loss [6]. In turn, apoptotic death of RGCs inAddress correspondence to these authors in the Faculty of Veterinary Medicine, University of Teramo, 64100 Teramo, Italy; Tel: 39 0861 266842; E mail: [email protected] and also the Division of Medicine, Campus BioMedico University of Rome, 00128 Rome, Italy; Tel: 39 06 225419169; Email: [email protected] 1570159X/18 58.00.glaucoma is because of different defects within the connection among central nervous program (CNS) and retina, including faults of reactive glia, synaptic connectivity and axonal transport, neurotrophic factor deprivation, proapoptotic signaling activation of neurotransmitters and neuromodulators, also as excitotoxicity and oxidative anxiety [7, 8]. In addition to glaucoma, RGC neurodegeneration happens in a number of other ocular Sibutramine hydrochloride Neuronal Signaling pathologies for example diabetic retinopathy (DR), agerelated macular degeneration (AMD) and some inherited retinal problems also as in Alzheimer’s disease and Parkinson’s illness, exactly where the retina seems to become an early web page of harm [911]. However, indicators of pigmentary retinopathy and degeneration of retinal nerve fibers have been identified in one more type of neurodegenerative disorder generally known as autosomal dominant cerebellar ataxias [12, 13]. Other regions potentially impacted are retinal microvessels, in DR [14], and retinal pigment epithelium (RPE) and photoreceptors, collectively with vascular and RGC damages, in AMD [15, 16].018 Bentham Science Publishers960 Current Neuropharmacology, 2018, Vol. 16, No.Rapino et al.So far essentially the most successful intervention used to block glaucoma progression could be the administration of drugs capable of lowering IOP, despite the fact that numerous sufferers have IOP inside the normal range and illness progression can continue even when IOP is correctly lowered [17, 18]. In addition, glaucomatous damage will not be limited towards the eye, nevertheless it also requires central visual pathways and vascular ailments on the CNS [19]. Certainly, neurodegeneration in glaucoma shares numerous pathway elements with other retinal and nonretinal neurodegenerative ailments, in order that an innovative therapeutic approach is now to help keep RGCs and photoreceptors alive to prevent irreversible damage of optic nerve, also as synaptic connectivity and retinal microvascular alterations [20, 21]. Interestingly, the five most common classes of drugs applied topically to lower IOP (2agonists, antagonists/blockers, prostaglandin analogs, carbonic anhydrase and cholinergic agents) possess an indirect neuroprotective action on the retina and/or optic nerve, by triggering mechanisms that consist of neuronal, glial and vascular pathways [2224]. However, lots of prospective biochemical pathways are activated in a receptordependent or independent manner by numerous organic and synthetic compounds, that directly supply neuroprotection: Aboral end wnt Inhibitors MedChemExpress antioxida.