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Updated: Nov 7, 2025

A Protocol for the Use of Remotely-Supervised Transcranial Direct Current Stimulation tDCS in Multiple Sclerosis MS
Published on: December 26, 2015
Citicoline: A Candidate for Adjunct Treatment of Multiple Sclerosis
Paweł Grieb1, Maciej Świątkiewicz1, Agnieszka Kamińska2
1Department of Experimental Pharmacology, Mossakowski Medical Research Institute, Polish Academy of Sciences, 02-106 Warsaw, Poland.
Citicoline shows promise in promoting myelin repair, an unmet need for multiple sclerosis (MS) patients. This nootropic agent demonstrated efficacy in rodent models of MS and warrants further investigation for supporting remyelination in human patients.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Remitting-relapsing multiple sclerosis (RR-MS) involves autoimmune attacks on myelin, followed by repair attempts.
- Current disease-modifying therapies (DMTs) primarily target myelin damage and often exhibit toxicity.
- Enhancing myelin repair is a critical unmet need in MS management.
Purpose of the Study:
- To investigate the potential of citicoline as a therapeutic agent for promoting myelin repair in multiple sclerosis (MS).
- To evaluate citicoline's efficacy in preclinical models relevant to MS pathology.
Main Methods:
- Citicoline was tested in experimental autoimmune encephalomyelitis (EAE) and cuprizone-induced demyelination rodent models.
- Visual evoked potentials (VEPs) in glaucoma patients, an indicator of neural pathway function, were assessed following citicoline treatment.
Main Results:
- Citicoline demonstrated significant efficacy in both EAE and cuprizone-induced rodent models of MS.
- Citicoline treatment improved VEPs in glaucoma patients, suggesting potential benefits for neural pathway function relevant to MS.
Conclusions:
- Citicoline exhibits potential as a myelin repair-enhancing agent for multiple sclerosis (MS).
- Its efficacy in preclinical models and positive effects on VEPs suggest further clinical evaluation for MS remyelination is warranted.
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