“…21 In a study by Schatz et al, 36 TES before mild light exposure temporarily preserved b-wave amplitudes and outer segment length, and reduced photoreceptor cell death after 2 weeks. The effects observed in this study were minor compared to the effects reported by Ni et al, 26 where TES sessions were repeated and different electrode configurations were used. In a rabbit model of rhodopsin mutations that mimic RP, TES resulted in both increased photoreceptor survival and improved retinal function.…”
Section: Tes In Animal Modelscontrasting
confidence: 65%
“…Enhanced survival of RGCs has also been observed after optic nerve crush, 15,16,20,32 after light-induced retinal damage, 26 and in ischemic rat retinas. 33 Tagami et al 32 revealed that the increased survival of RGCs was in accordance with the number of TES applications and that the daily application of TES exhibited the most effect.…”
Section: Tes In Animal Modelsmentioning
confidence: 88%
“…However, beneficial effects of ES have been shown in one study using transorbital ES 14 and in several animal experiments using TES (Table 1). 15e35 These studies can be categorized as follows: i) healthy animals 17e19, 23,26,31,34 ; ii) transgenic animals 22,28 ; iii) animals as a disease model for RP 21 ; iv) animals with induced ischemic insult, 27,29,33 optic nerve crush, 15,16,20,32 and transected optic nerve 24,25 ; and v) animal cells isolated from the retina. 35 …”
Evolving research has provided evidence that noninvasive electrical stimulation (ES) of the eye may be a promising therapy for either preserving or restoring vision in several retinal and optic nerve diseases. In this review, we focus on minimally invasive strategies for the delivery of ES and accordingly summarize the current literature on transcorneal, transorbital, and transpalpebral ES in both animal experiments and clinical studies. Various mechanisms are believed to underlie the effects of ES, including increased production of neurotrophic agents, improved chorioretinal blood circulation, and inhibition of proinflammatory cytokines. Different animal models have demonstrated favorable effects of ES on both the retina and the optic nerve. Promising effects of ES have also been demonstrated in clinical studies; however, all current studies have a lack of randomization and/or a control group (sham). There is thus a pressing need for a deeper understanding of the underlying mechanisms that govern clinical success and optimization of stimulation parameters in animal studies. In addition, such research should be followed by large, prospective, clinical studies to explore the full potential of ES. Through this review, we aim to provide insight to guide future research on ES as a potential therapy for improving vision. (Am J Pathol 2016 http://dx
“…21 In a study by Schatz et al, 36 TES before mild light exposure temporarily preserved b-wave amplitudes and outer segment length, and reduced photoreceptor cell death after 2 weeks. The effects observed in this study were minor compared to the effects reported by Ni et al, 26 where TES sessions were repeated and different electrode configurations were used. In a rabbit model of rhodopsin mutations that mimic RP, TES resulted in both increased photoreceptor survival and improved retinal function.…”
Section: Tes In Animal Modelscontrasting
confidence: 65%
“…Enhanced survival of RGCs has also been observed after optic nerve crush, 15,16,20,32 after light-induced retinal damage, 26 and in ischemic rat retinas. 33 Tagami et al 32 revealed that the increased survival of RGCs was in accordance with the number of TES applications and that the daily application of TES exhibited the most effect.…”
Section: Tes In Animal Modelsmentioning
confidence: 88%
“…However, beneficial effects of ES have been shown in one study using transorbital ES 14 and in several animal experiments using TES (Table 1). 15e35 These studies can be categorized as follows: i) healthy animals 17e19, 23,26,31,34 ; ii) transgenic animals 22,28 ; iii) animals as a disease model for RP 21 ; iv) animals with induced ischemic insult, 27,29,33 optic nerve crush, 15,16,20,32 and transected optic nerve 24,25 ; and v) animal cells isolated from the retina. 35 …”
Evolving research has provided evidence that noninvasive electrical stimulation (ES) of the eye may be a promising therapy for either preserving or restoring vision in several retinal and optic nerve diseases. In this review, we focus on minimally invasive strategies for the delivery of ES and accordingly summarize the current literature on transcorneal, transorbital, and transpalpebral ES in both animal experiments and clinical studies. Various mechanisms are believed to underlie the effects of ES, including increased production of neurotrophic agents, improved chorioretinal blood circulation, and inhibition of proinflammatory cytokines. Different animal models have demonstrated favorable effects of ES on both the retina and the optic nerve. Promising effects of ES have also been demonstrated in clinical studies; however, all current studies have a lack of randomization and/or a control group (sham). There is thus a pressing need for a deeper understanding of the underlying mechanisms that govern clinical success and optimization of stimulation parameters in animal studies. In addition, such research should be followed by large, prospective, clinical studies to explore the full potential of ES. Through this review, we aim to provide insight to guide future research on ES as a potential therapy for improving vision. (Am J Pathol 2016 http://dx
“…They have also collected evidence for enhanced survival of ganglion cells after optic nerve injury [9][10][11][12][13] (crush or axotomy), for increased survival of different retinal cell populations after light-induced retinal damage [14,15], and for increased cell survival in ischemic rat retinas [16]. Likely mechanisms, elucidated in these experiments, include advantageous regulation of neurotrophins such as endogenous insulin-like growth factor (IGF)-1 [10,14,17] and Fgf2 [18], involvement of B-cell lymphoma 2 (Bcl-2)…”
Section: Animal Experimentsmentioning
confidence: 99%
“…protein and co-factors of the BAX family [19], members of the tumor necrosis factor family [19], ciliary neurotrophic factor (CNTF), and brain-derived neurotrophic factor (BDNF) [14].…”
Visual impairment caused by optic neuropathies is irreversible because retinal ganglion cells (RGCs), the specialized neurons of the retina, do not have the capacity for self‐renewal and self‐repair. Blindness caused by optic nerve neuropathies causes extensive physical, financial, and social consequences in human societies. Recent studies on different animal models and humans have established effective strategies to prevent further RGC degeneration and replace the cells that have deteriorated. In this review, we discuss the application of electrical stimulation (ES) and magnetic field stimulation (MFS) in optic neuropathies, their mechanisms of action, their advantages, and limitations. ES and MFS can be applied effectively in the field of neuroregeneration.. Although stem cells are becoming a promising approach for regenerating RGCs, the inhibitory environment of the CNS and the long visual pathway from the optic nerve to the superior colliculus are critical barriers to overcome. Scientific evidence has shown that adjuvant treatments, such as the application of ES and MFS help direct thetransplanted RGCs to extend their axons and form new synapses in the central nervous system (CNS). In addition, these techniques improve CNS neuroplasticity and decrease the inhibitory effects of the CNS. Possible mechanisms mediating the effects of electrical current on biological tissues include the release of anti‐inflammatory cytokines, improvement of microcirculation, stimulation of cell metabolism, and modification of stem cell function. ES and MFS have the potential to promote angiogenesis, direct axon growth toward the intended target, and enhance appropriate synaptogenesis in optic nerve regeneration.
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