Coma, retinal diseases, retinal ganglion cells, endocannabinoids, phytocannabinoids. 1. INTRODUCTION: GLAUCOMA AND RETINAL NEURODEGENERATION Glaucoma comprises a group of eye issues which can cause progressive and/or irreversible blindness. It impacts the elderly but is becoming extra widespread also amongst younger men and women and also kids [1, 2]. Glaucoma is normally brought on by enhanced intraocular stress (IOP), while other components are involved like progressive harm of retinal ganglion cells (RGCs), referred to as “the messengers of retina”, leading to optic nerve degeneration [35]. These situations bring about distinct visual field defects, and eventually comprehensive 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; Email: [email protected] and also the Division of Medicine, Campus BioMedico University of Rome, 00128 Rome, Italy; Tel: 39 06 225419169; E mail: [email protected] 1570159X/18 58.00.glaucoma is resulting from distinct defects inside the connection among central nervous method (CNS) and retina, like faults of reactive glia, synaptic connectivity and axonal transport, neurotrophic element deprivation, proapoptotic signaling activation of neurotransmitters and neuromodulators, at the same time as excitotoxicity and oxidative pressure [7, 8]. Apart from glaucoma, RGC neurodegeneration occurs in various other ocular pathologies which include diabetic retinopathy (DR), agerelated macular degeneration (AMD) and a few inherited retinal disorders as well as in Chlorobutanol manufacturer Alzheimer’s illness and Parkinson’s illness, where the retina appears to be an early web site of harm [911]. Yet, signs of pigmentary retinopathy and degeneration of retinal nerve fibers have been identified in yet another kind of neurodegenerative disorder generally known as autosomal dominant cerebellar ataxias [12, 13]. Other locations potentially affected 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 Present Neuropharmacology, 2018, Vol. 16, No.Rapino et al.So far essentially the most powerful intervention employed to block glaucoma progression is the administration of drugs capable of lowering IOP, even though numerous patients have IOP within the typical variety and disease progression can continue even when IOP is properly lowered [17, 18]. Additionally, glaucomatous harm is not limited to the eye, but it also requires central visual pathways and vascular ailments with the CNS [19]. Indeed, neurodegeneration in glaucoma shares many pathway components with other retinal and nonretinal neurodegenerative illnesses, so that an innovative therapeutic method is now to help keep RGCs and photoreceptors alive to avoid irreversible damage of optic nerve, at the same time as synaptic connectivity and retinal microvascular alterations [20, 21]. Interestingly, the 5 most common classes of drugs employed topically to reduced 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 incorporate neuronal, glial and vascular pathways [2224]. On the other hand, quite a few potential biochemical pathways are activated inside a receptordependent or independent manner by several natural and synthetic compounds, that directly supply neuroprotection: antioxida.
