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The Emerging Role of Exosome Nanoparticles in Regenerative Medicine
Published in Harishkumar Madhyastha, Durgesh Nandini Chauhan, Nanopharmaceuticals in Regenerative Medicine, 2022
Zahra Sadat Hashemi, Mahlegha Ghavami, Saeed Khalili, Seyed Morteza Naghib
Studies also supported the effectiveness of BMSC-derived exosomes for traumatic and degenerative ocular diseases. Traumatic (optic neuropathy) and degenerative (glaucoma) eye diseases, which cause irreversible blindness, are the results of the loss and dysfunction of retinal ganglion cells (RGC) and their axons. The neuroprotective and axogenic effects of MSCs have been well-established on RGC models (Mead et al. 2015). Further research conducted by this group has suggested that BMSC-derived exosomes may be beneficial for the survival of RGCs via miRNA-dependent mechanisms in a rodent optic nerve crush (ONC) model (Mead and Tomarev 2017).
Biochemical Markers in Ophthalmology
Published in Ching-Yu Cheng, Tien Yin Wong, Ophthalmic Epidemiology, 2022
Abdus Samad Ansari, Pirro G. Hysi
Disease-associated genes often share basic functional properties, whose study can inform about disease mechanisms. There are many functional gene sets that are statistically enriched among the GWAS-identified POAG genes. One very enriched set of functional properties among POAG-associated genes is the cell cycle, cell division, inhibition, and apoptosis [53, 63]. These genes tend to be associated with endophenotypes underlying optic disc morphology features, such as VCDR, disc and rim areas. This seems to suggest that retinal ganglion cell vitality may be a mechanism leading to glaucoma. The presence of such a strong link between cell division inhibition and POAG points to potentially new and transformative pharmacological POAG treatments that will aim to boost cells’ regenerative capabilities and resilience. This is interesting, as to date there is only one available therapeutical option with neuroprotective properties (brimonidine). Experimental intervention aimed at inhibiting cyclin-dependent kinases, a protein family, which also included the CDKN2B protein, whose production and activity are under strong genetic regulation in POAG, have shown neuroprotection and improved clinical outcomes [64, 65]. Extending these studies to human glaucoma patients may lead to the development of novel treatments against the disease.
Cranial Neuropathies II, III, IV, and VI
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Tanyatuth Padungkiatsagul, Heather E. Moss
This is a disorder of the cranial nerve (CN) II, or optic nerve resulting in visual disturbance when using the eye on the affected side. This can be perceived as blurred vision, decreased visual acuity, loss of certain part of vision (visual field defect), or abnormal perception of color (dyschromatopsia). Strictly speaking, the optic nerve extends from the eyeball to the chiasm. However, any disease that impacts the retinal ganglion cells (RGCs) including those of the optic chiasm and optic tract can have structural and functional effects on the optic nerves.
Can Nerve Growth Factor (NGF) Be a Treatment Option for Pediatric Eye Diseases?
Published in Seminars in Ophthalmology, 2023
Leyla Yavuz Saricay, Jose Efren Gonzalez Monroy, Anne B Fulton
Glaucoma is one of the most significant causes of blindness worldwide, which is characterized by progressive retinal ganglion cell degeneration and visual field constriction. It may occur with or without intraocular pressure elevation.43 The retinal ganglion cell apoptosis or the progressive degeneration of the optic nerve may be the cause of blindness. In recent clinical practice, one of the major targets of glaucoma therapy is to slow the retinal ganglion cell apoptosis and promote retinal ganglion cell survival in addition to the lowering of intraocular pressure. The neuroprotection of retinal ganglion cell apoptosis aims to prevent permanent nerve cell loss and sustain healthy neuronal functions as an important alternative approach for the treatment of glaucoma in addition to lowering the intraocular pressure.
Mimicking chronic glaucoma over 6 months with a single intracameral injection of dexamethasone/fibronectin-loaded PLGA microspheres
Published in Drug Delivery, 2022
Alba Aragón-Navas, María J. Rodrigo, David Garcia-Herranz, Teresa Martinez, Manuel Subias, Silvia Mendez, Jesús Ruberte, Judit Pampalona, Irene Bravo-Osuna, Julian Garcia-Feijoo, Luis E. Pablo, Elena Garcia-Martin, Rocío Herrero-Vanrell
Degenerative diseases of the retina begin with primary damage, for example of the axons of retinal ganglion cells in the case of glaucoma. When the damaged cell dies, it releases neurotoxic compounds in the vicinity that damage the adjacent neurons that also end up dying in what is known as “secondary neurodegeneration” (Ritch, 2000). Several decades ago, some researchers postulated the idea of “neuroprotection” as a complementary treatment in degenerative diseases (Weinreb & Levin, 1999). At the level of the retina neuroprotection can be defined as: “Prevention or slowing down of the loss of functional integrity of the cells of the retina, their axons and their axonal connections to maintain and stabilize the vision of patients as much as possible” (Ritch, 2000). Pardue et al. describe this neurodegeneration of the retina in 3 stages: an adaptive first step where there is only oxidative stress and neuronal dysfunction, a second stage, the “Early pathology”, where retinal structures begin to damage but still reversibly, and a third stage of "Late pathology" where blindness appears and where the damage is already irreversible. According to those authors, “starting neuroprotective treatments at the first signs of the retinal disease would provide the most benefit in preserving vision” (Pardue & Allen, 2018).
Neuro-Ophthalmic Literature Review
Published in Neuro-Ophthalmology, 2022
David A. Bellows, Noel C. Y. Chan, John J. Chen, Hui-Chen Cheng, Peter W. MacIntosh, Michael S. Vaphiades, Konrad P. Weber, Xiaojun Zhang
The authors enrolled 37 patients with WFS1-associated optic neuropathy (WON) to investigate the pattern of vision loss and genotype–phenotype correlations. They identified 22 recessive and five dominant WFS1 variants. WON patients had significant loss of the peripapillary retinal nerve fibre layer and ganglion cell layer-inner plexiform cell layer complex on optical coherence tomography. In 12 WON patients, who received visual electrophysiological testing, only two patients had normal pattern visual evoked potentials, while the rest had either delayed or undetectable responses. Advanced psychophysical testing indicated involvement of the major retinal ganglion cell (RGC) subpopulations. In addition, WON patients showed an accelerated rate of visual deterioration with increasing age. The dominant variants tended to cause less severe vision loss compared with the recessive WFS1 variants. The phenotype of recessive WFS1 variants ranged from isolated WON to severe multisystem disease, depending on the WFS1 alleles. The authors concluded that WFS1 variants result in heterogenous phenotypes influenced by the mode of inheritance and the disease-causing alleles, with biallelic WFS1 variants cause more variable, but generally more severe vision and RGC loss.