Glutamate transporter contribution to retinal ganglion cell vulnerability in a rat model of multiple sclerosis

Boccuni, Isabella; Bas-Orth, Carlos; Bruehl, Claus; Draguhn, Andreas; Fairless, Richard

doi:10.1016/j.nbd.2023.106306

Cited by 3 publications

(3 citation statements)

References 58 publications

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“…Downregulation of GLAST expression has been reported in human glaucomatous eyes ( Naskar et al, 2000 ) and mutations in GLAST are also found in glaucoma patients ( Yanagisawa et al, 2020 ). Consistently, overexpression of Glast by AAV transduction protects retinal ganglion cells from degeneration in experimental autoimmune encephalomyelitis rats ( Boccuni et al, 2023 ), highlighting a protective role of MG on photoreceptors.…”

Section: Mg-photoreceptor Interaction In Irdmentioning

confidence: 80%

Cell-cell interaction in the pathogenesis of inherited retinal diseases

Du,

Butler,

Chen

2024

Front. Cell Dev. Biol.

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The retina is part of the central nervous system specialized for vision. Inherited retinal diseases (IRD) are a group of clinically and genetically heterogenous disorders that lead to progressive vision impairment or blindness. Although each disorder is rare, IRD accumulatively cause blindness in up to 5.5 million individuals worldwide. Currently, the pathophysiological mechanisms of IRD are not fully understood and there are limited treatment options available. Most IRD are caused by degeneration of light-sensitive photoreceptors. Genetic mutations that abrogate the structure and/or function of photoreceptors lead to visual impairment followed by blindness caused by loss of photoreceptors. In healthy retina, photoreceptors structurally and functionally interact with retinal pigment epithelium (RPE) and Müller glia (MG) to maintain retinal homeostasis. Multiple IRD with photoreceptor degeneration as a major phenotype are caused by mutations of RPE- and/or MG-associated genes. Recent studies also reveal compromised MG and RPE caused by mutations in ubiquitously expressed ciliary genes. Therefore, photoreceptor degeneration could be a direct consequence of gene mutations and/or could be secondary to the dysfunction of their interaction partners in the retina. This review summarizes the mechanisms of photoreceptor-RPE/MG interaction in supporting retinal functions and discusses how the disruption of these processes could lead to photoreceptor degeneration, with an aim to provide a unique perspective of IRD pathogenesis and treatment paradigm. We will first describe the biology of retina and IRD and then discuss the interaction between photoreceptors and MG/RPE as well as their implications in disease pathogenesis. Finally, we will summarize the recent advances in IRD therapeutics targeting MG and/or RPE.

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Section: Mg-photoreceptor Interaction In Irdmentioning

confidence: 80%

Cell-cell interaction in the pathogenesis of inherited retinal diseases

Du,

Butler,

Chen

2024

Front. Cell Dev. Biol.

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“…Glutamatergic neurotransmission is responsible for many cognitive, motor, sensory, and autonomic nervous activities [ 220 , 221 , 222 ]. Neuroexcitotoxicity induced by glutamate has been demonstrated in a number of neurological and psychiatric disorders, including PD [ 223 , 224 , 225 , 226 , 227 ], epilepsy [ 228 , 229 ], traumatic brain injury [ 230 , 231 ], MS [ 232 , 233 , 234 ], AD [ 223 , 224 , 235 , 236 ], HD [ 223 , 237 , 238 , 239 ], ALS [ 223 , 239 , 240 ], etc.…”

Section: Resultsmentioning

confidence: 99%

L-Carnitine in the Treatment of Psychiatric and Neurological Manifestations: A Systematic Review

Wang,

Pan,

Liu

et al. 2024

Nutrients

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L-carnitine (LC), a vital nutritional supplement, plays a crucial role in myocardial health and exhibits significant cardioprotective effects. LC, being the principal constituent of clinical-grade supplements, finds extensive application in the recovery and treatment of diverse cardiovascular and cerebrovascular disorders. However, controversies persist regarding the utilization of LC in nervous system diseases, with varying effects observed across numerous mental and neurological disorders. This article primarily aims to gather and analyze database information to comprehensively summarize the therapeutic potential of LC in patients suffering from nervous system diseases while providing valuable references for further research. Methods: A comprehensive search was conducted in PubMed, Web Of Science, Embase, Ovid Medline, Cochrane Library and Clinicaltrials.gov databases. The literature pertaining to the impact of LC supplementation on neurological or psychiatric disorders in patients was reviewed up until November 2023. No language or temporal restrictions were imposed on the search. Results: A total of 1479 articles were retrieved, and after the removal of duplicates through both automated and manual exclusion processes, 962 articles remained. Subsequently, a meticulous re-screening led to the identification of 60 relevant articles. Among these, there were 12 publications focusing on hepatic encephalopathy (HE), while neurodegenerative diseases (NDs) and peripheral nervous system diseases (PNSDs) were represented by 9 and 6 articles, respectively. Additionally, stroke was addressed in five publications, whereas Raynaud’s syndrome (RS) and cognitive disorder (CD) each had three dedicated studies. Furthermore, migraine, depression, and amyotrophic lateral sclerosis (ALS) each accounted for two publications. Lastly, one article was found for other symptoms under investigation. Conclusion: In summary, LC has demonstrated favorable therapeutic effects in the management of HE, Alzheimer’s disease (AD), carpal tunnel syndrome (CTS), CD, migraine, neurofibromatosis (NF), PNSDs, RS, and stroke. However, its efficacy appears to be relatively limited in conditions such as ALS, ataxia, attention deficit hyperactivity disorder (ADHD), depression, chronic fatigue syndrome (CFS), Down syndrome (DS), and sciatica.

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“…The pathophysiology of ON in MOGAD is particularly interesting as MOG is not expressed in the retina [39]. Other mechanisms have been proposed to contribute to retinal ganglion cell degeneration, such as glutamate cytotoxicity [40], as well as the lack of classical blood-brain barrier characteristics of the optic nerve head [41].…”

Section: Historical Evolution and Pathophysiology Of Mogad In Human D...mentioning

confidence: 99%

MOG antibody-associated optic neuritis

Jeyakumar,

Lerch,

Dale

et al. 2024

Eye

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Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is a demyelinating disorder, distinct from multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD). MOGAD most frequently presents with optic neuritis (MOG-ON), often with characteristic clinical and radiological features. Bilateral involvement, disc swelling clinically and radiologically, and longitudinally extensive optic nerve hyperintensity with associated optic perineuritis on MRI are key characteristics that can help distinguish MOG-ON from optic neuritis due to other aetiologies. The detection of serum MOG immunoglobulin G utilising a live cell-based assay in a patient with a compatible clinical phenotype is highly specific for the diagnosis of MOGAD. This review will highlight the key clinical and radiological features which expedite diagnosis, as well as ancillary investigations such as visual fields, visual evoked potentials and cerebrospinal fluid analysis, which may be less discriminatory. Optical coherence tomography can identify optic nerve swelling acutely, and atrophy chronically, and may transpire to have utility as a diagnostic and prognostic biomarker. MOG-ON appears to be largely responsive to corticosteroids, which are often the mainstay of acute management. However, relapses are common in patients in whom follow-up is prolonged, often in the context of early or rapid corticosteroid tapering. Establishing optimal acute therapy, the role of maintenance steroid-sparing immunotherapy for long-term relapse prevention, and identifying predictors of relapsing disease remain key research priorities in MOG-ON.

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Glutamate transporter contribution to retinal ganglion cell vulnerability in a rat model of multiple sclerosis

Cited by 3 publications

References 58 publications

Cell-cell interaction in the pathogenesis of inherited retinal diseases

Cell-cell interaction in the pathogenesis of inherited retinal diseases

L-Carnitine in the Treatment of Psychiatric and Neurological Manifestations: A Systematic Review

MOG antibody-associated optic neuritis

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