Neuroprotection for acute optic neuritis—Can it work?

Raftopoulos, Rhian; Kapoor, Raju

doi:10.1016/j.msard.2013.02.001

Cited by 12 publications

(13 citation statements)

References 27 publications

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“…It has been shown in experimental animal models that loading of partially demyelinated axons with sodium ions results in an accumulation of calcium ions, which triggers a cascade of degradative enzyme activity and finally leads to axonal degeneration [107]. Partial blockade of sodium channels is therefore thought to have neuroprotective properties [107][108][109].…”

Section: Phenytoin and Oxcarbazepinementioning

confidence: 99%

“…Partial blockade of sodium channels is therefore thought to have neuroprotective properties [107][108][109]. As such, sodium-blocking agents such as phenytoin, lamotrigine, carbamazepine, or oxcarbazepine, and even newer agents such as safinamide and flecainide have been suggested to have potential neuroprotective effects in MS [109].…”

Section: Phenytoin and Oxcarbazepinementioning

confidence: 99%

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Therapeutic Advances and Future Prospects in Progressive Forms of Multiple Sclerosis

2016

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Identifying effective therapies for the treatment of progressive forms of multiple sclerosis (MS) is a highly relevant priority and one of the greatest challenges for the global MS community. Better understanding of the mechanisms involved in progression of the disease, novel trial designs, drug repurposing strategies, and new models of collaboration may assist in identifying effective therapies. In this review, we discuss various therapies under study in phase II or III trials, including antioxidants (idebenone); tyrosine kinase inhibitors ( m a s i t i n i b ) ; s p h i n g o s i n e r e c e p t o r m o d u l a t o r s (siponimod); monoclonal antibodies (anti-leucine-rich repeat and immunoglobulin-like domain containing neurite outgrowth inhibitor receptor-interacting protein-1, natalizumab, ocrelizumab, intrathecal rituximab); hematopoetic stem cell therapy; statins and other possible neuroprotective agents (amiloride, riluzole, fluoxetine, oxcarbazepine); lithium; phosphodiesterase inhibitors (ibudilast); hormone-based therapies (adrenocorticotrophic hormone and erythropoietin); T-cell receptor peptide vaccine (NeuroVax); autologous T-cell immunotherapy (Tcelna); MIS416 (a microparticulate immune response modifier); dopamine antagonists (domperidone); and nutritional supplements, including lipoic acid, biotin, and sunphenon epigallocatechin-3-gallate (green tea extract). Given ongoing and planned clinical trial initiatives, and the largest ever focus of the global research community on progressive MS, future prospects for developing targeted therapeutics aimed at reducing disability in progressive forms of MS appear promising.

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Section: Phenytoin and Oxcarbazepinementioning

confidence: 99%

Section: Phenytoin and Oxcarbazepinementioning

confidence: 99%

Therapeutic Advances and Future Prospects in Progressive Forms of Multiple Sclerosis

2016

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“…Statins (hydroxymethylglutaryl-CoA reductase inhibitors) have been studied for their immunomodulatory and neuroprotective effects that they probably exercise through the improvement of cerebrovascular hemodynamics [91]. Moreover, Simvastatin seems to significantly reduce brain atrophy when compared with placebo, as showed recently a II phase trial [92].…”

Section: Therapeutic Advances and Future Prospects In Progressive mentioning

confidence: 99%

A Personalized Approach in Progressive Multiple Sclerosis: The Current Status of Disease Modifying Therapies (DMTs) and Future Perspectives

D’Amico

Patti

Zanghì

et al. 2016

IJMS

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Using the term of progressive multiple sclerosis (PMS), we considered a combined population of persons with secondary progressive MS (SPMS) and primary progressive MS (PPMS). These forms of MS cannot be challenged with efficacy by the licensed therapy. In the last years, several measures of risk estimation were developed for predicting clinical course in MS, but none is specific for the PMS forms. Personalized medicine is a therapeutic approach, based on identifying what might be the best therapy for an individual patient, taking into account the risk profile. We need to achieve more accurate estimates of useful predictors in PMS, including unconventional and qualitative markers which are not yet currently available or practicable routine diagnostics. The evaluation of an individual patient is based on the profile of disease activity.Within the neurology field, PMS is one of the fastest-moving going into the future.

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“…Other strategies in clinical phases include the use of trophic factor compounds (eritropoietin, BN201), antioxidant compounds (the green tea extract epigallocatechin-3-gallate, ginkgo biloba extracts, biotin, dimethyl-fumarate, olexosime), modulating estrogen receptors, metabolites (dimethyl-fumarate, methyltioadenosine), blocking semaphorins (VX15/2503), and ion channels modulators (carbamacepin, phenytoin, lamotrigin, amiloride, riluzole) ( Table 2) [21,70]. All these drugs still need to show their efficacy in phase 3 trials and then define how they would be integrated in the MS armamentarium, probably as a combination therapy with immunomodulators for relapsing MS or perhaps in combination with different agents for progressive MS.…”

Section: Neuroprotective Therapies Under Development For Ms and Othermentioning

confidence: 99%

Neuroprotective therapies for multiple sclerosis and other demyelinating diseases

Villoslada

2016

Mult Scler Demyelinating Disord

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Damage to the Central Nervous Systems (CNS) in Multiple Sclerosis (MS) seems to be mainly due to chronic inflammation of the CNS with superimposed bouts of inflammatory activity by the adaptive immune system. The immune mediated damage can be amplified by neurodegenerative mechanisms in damaged axons including anterograde or retrograde axonal or transynaptic degeneration, synaptic pruning and neuronal or oligodendrocyte death. As such, it is highly unlikely that CNS damage can be prevented using only immunomodulatory drugs. For this reason, neuroprotection, aimed at preventing axonal, neuronal, myelin, and oligodendrocyte damage and cell death in the presence of this toxic microenvironment is highly pursued in MS and other demyelinating diseases. Neuroprotective strategies target different processes including oxidative stress, ionic imbalance (sodium, potassium or calcium), energy depletion, trophic factor support, metabolites balance, excitotoxicity, apoptosis, remyelination, etc. Although none of these strategies have translated into approved drugs to date, improvement in the understanding of underlying biology, in the design of clinical trials specific for assessing neuroprotection, and new technologies for developing novel therapies for neuroprotection suggest a new avenue for treating MS, Optic Neuritis or Neuromyelitis Optica (NMO). Several of these therapies are now entering clinical phases and if successful, such strategies would improve patients' quality of life, and will be even more critical for patients with progressive MS. In the event that such therapies target natural repair mechanisms rather than disease specific processes, they can potentially be useful for other brain diseases such as stroke, neurodegenerative diseases, brain trauma or epilepsy.

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Neuroprotection for acute optic neuritis—Can it work?

Cited by 12 publications

References 27 publications

Therapeutic Advances and Future Prospects in Progressive Forms of Multiple Sclerosis

Therapeutic Advances and Future Prospects in Progressive Forms of Multiple Sclerosis

A Personalized Approach in Progressive Multiple Sclerosis: The Current Status of Disease Modifying Therapies (DMTs) and Future Perspectives

Neuroprotective therapies for multiple sclerosis and other demyelinating diseases

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