Transcorneal Electrical Stimulation Reduces Neurodegenerative Process in a Mouse Model of Glaucoma

Jassim, Assraa Hassan; Cavanaugh, McKay; Shah, Jessica Stukel; Willits, Rebecca Kuntz; Inman, Denise M.

doi:10.1007/s10439-020-02608-8

Cited by 16 publications

(19 citation statements)

References 40 publications

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“…In an in vitro model of light-induced photoreceptor degeneration, electrical stimulation was shown to suppress the activation of microglia, which in turn inhibited the secretion of pro-inflammatory interleukin (IL)-1β and the tumour necrosis factor (TNF)-α, leading to decreased photoreceptor cell death [ 39 ]. These results were consistent with rodent experiments that showed that TES had immunomodulatory effects in suppressing retinal microglial activation after acute ocular hypertensive injury [ 42 ], optic nerve transection [ 43 ], and in a glaucoma model [ 44 ]. The improvement in RGC survival was accompanied by the upregulation of the anti-inflammatory cytokine IL-10 and the reduction of pro-inflammatory factors IL-6, TNF-α, and cyclooxygenase-2 [ 42 , 43 ].…”

Section: Mechanisms Of Action Of Tessupporting

confidence: 90%

“…The research team later demonstrated that the repeated administration of TES at optimal stimulation parameters (pulse width: 1 or 2 ms/phase; stimulation amplitude: 100 or 200 μA; stimulation frequency: 1, 5, or 20 Hz; stimulation duration: >30 min) after optic nerve injury in rats provided the best neuroprotection and led to the regeneration of retinal axons [ 35 , 63 ]. Concordantly, the neuroprotective effects of TES on RGCs were also shown in rodent models of optic nerve crush [ 64 , 65 , 66 ], non-arteritic ischaemic optic neuropathy [ 67 ], ischaemic retinas [ 48 ], acute ocular hypertensive injury [ 42 ], and glaucoma [ 44 ]. The therapeutic applications of TES were not limited to preserving RGCs and their axons.…”

Section: Application Of Tes In Ophthalmologymentioning

confidence: 90%

“…Contact-lens-like electrodes are placed on the corneas of subjects and connected to a stimulator and stimulus isolator unit, while an inactive reference electrode is connected to the skin surrounding the eye [ 27 ]. This has been shown to have beneficial effects on the retina and optic nerve, leading to visual improvements in both preclinical [ 34 , 35 , 36 , 42 , 44 , 48 , 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 ] and clinical settings [ 71 , 72 , 73 , 74 , 75 , 76 ].…”

Section: Application Of Tes In Ophthalmologymentioning

confidence: 99%

“…Moreover, ECT was also reported to increase the level of blood IL-10 [ 115 ], which is a well-established anti-inflammatory cytokine that prevents neuronal and glial cell death [ 128 ]. Given that TES was demonstrated to reduce inflammatory responses via regulating cytokine expression and suppressing microglial activation [ 39 , 42 , 43 , 44 ], its putative anti-depressant effects on inflammation warrant investigation in the future.…”

Section: Comparison Of Fda-approved Treatments For Major Depressionmentioning

confidence: 99%

“…Although the modulation effects of TES in these non-visual brain regions have yet to be confirmed, both PFC and PHG are involved in mood alterations [ 32 ], suggesting that TES may have a role in regulating emotion. The potential neuroprotective properties of TES are possibly achieved through regulating neuroplasticity [ 30 , 33 ], neurotrophic expression [ 34 , 35 , 36 , 37 , 38 , 39 , 40 ], inflammatory responses [ 39 , 41 , 42 , 43 , 44 ], apoptosis [ 36 , 45 , 46 , 47 ], glutamate metabolism [ 48 ], and retinal blood flow [ 49 , 50 ]. The putative neuroprotective effects of TES on mood control are further supported by its shared mechanisms of action with current antidepressant treatments, including its neuroprotective effects against apoptosis and inflammation, as well as its ability to promote neurotrophic expression.…”

Section: Introductionmentioning

confidence: 99%

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Neuroprotective Effects and Therapeutic Potential of Transcorneal Electrical Stimulation for Depression

Kwon

Agadagba

et al. 2021

Cells

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Transcorneal electrical stimulation (TES) has emerged as a non-invasive neuromodulation approach that exerts neuroprotection via diverse mechanisms, including neurotrophic, neuroplastic, anti-inflammatory, anti-apoptotic, anti-glutamatergic, and vasodilation mechanisms. Although current studies of TES have mainly focused on its applications in ophthalmology, several lines of evidence point towards its putative use in treating depression. Apart from stimulating visual-related structures and promoting visual restoration, TES has also been shown to activate brain regions that are involved in mood alterations and can induce antidepressant-like behaviour in animals. The beneficial effects of TES in depression were further supported by its shared mechanisms with FDA-approved antidepressant treatments, including its neuroprotective properties against apoptosis and inflammation, and its ability to enhance the neurotrophic expression. This article critically reviews the current findings on the neuroprotective effects of TES and provides evidence to support our hypothesis that TES possesses antidepressant effects.

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Section: Mechanisms Of Action Of Tessupporting

confidence: 90%

Section: Application Of Tes In Ophthalmologymentioning

confidence: 90%

Section: Application Of Tes In Ophthalmologymentioning

confidence: 99%

Section: Comparison Of Fda-approved Treatments For Major Depressionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Neuroprotective Effects and Therapeutic Potential of Transcorneal Electrical Stimulation for Depression

Kwon

Agadagba

et al. 2021

Cells

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Application of electrostimulation and magnetic stimulation in patients with optic neuropathy: A mechanistic review

Khalili,

Shadmani,

Sanie‐Jahromi

2024

Developmental Neurobiology

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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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Vascular dysregulation in glaucoma: retinal vasoconstriction and normal neurovascular coupling in altitudinal visual field defects

Zhou

Sabel²

2023

EPMA Journal

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Purpose Vision loss in glaucoma is not only associated with elevated intraocular pressure and neurodegeneration, but vascular dysregulation (VD) is a major factor. To optimize therapy, an improved understanding of concepts of predictive, preventive, and personalized medicine (3PM) is needed which is based on a more detailed understanding of VD pathology. Specifically, to learn if the root cause of glaucomatous vision loss is of neuronal (degeneration) or vascular origin, we now studied neurovascular coupling (NVC) and vessel morphology and their relationship to vision loss in glaucoma. Methods In patients with primary open angle glaucoma (POAG) (n = 30) and healthy controls (n = 22), NVC was studied using dynamic vessel analyzer to quantify retinal vessel diameter before, during, and after flicker light stimulation to evaluate the dilation response following neuronal activation. Vessel features and dilation were then related to branch level and visual field impairment. Results Retinal arterial and venous vessels had significantly smaller diameters in patients with POAG in comparison to controls. However, both arterial and venous dilation reached normal values during neuronal activation despite their smaller diameters. This was largely independent of visual field depth and varied among patients. Conclusions Because dilation/constriction is normal, VD in POAG can be explained by chronic vasoconstriction which limits energy supply to retinal (and brain) neurons with subsequent hypo-metabolism (“silent” neurons) or neuronal cell death. We propose that the root cause of POAG is primarily of vascular and not neuronal origin. This understanding can help to better personalize POAG therapy of not only targeting eye pressure but also vasoconstriction to prevent low vision, slowing its progression and supporting recovery and restoration. Trial registration ClinicalTrials.gov, # NCT04037384 on July 3, 2019.

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Transcorneal Electrical Stimulation Reduces Neurodegenerative Process in a Mouse Model of Glaucoma

Cited by 16 publications

References 40 publications

Neuroprotective Effects and Therapeutic Potential of Transcorneal Electrical Stimulation for Depression

Neuroprotective Effects and Therapeutic Potential of Transcorneal Electrical Stimulation for Depression

Application of electrostimulation and magnetic stimulation in patients with optic neuropathy: A mechanistic review

Vascular dysregulation in glaucoma: retinal vasoconstriction and normal neurovascular coupling in altitudinal visual field defects

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