Pharmacological treatment for memory disorder in multiple sclerosis

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Multiple sclerosis (MS) is an autoimmune, neurodegenerative, inflammatory disorder that affects nerve fibers of the central nervous system.1 Myelin, the protective sheath surrounding nerve fibers, becomes damaged by immune-mediated destruction, resulting in demyelination and axonal as well as neuronal loss in the central nervous system. Demyelination and axonal as well as neuronal loss are believed to contribute to MS-related cognitive impairment. Memory disorder is one of the most frequent cognitive impairments in MS, with estimates suggesting that 40–65% of individuals are affected. Typically, long-term and working memories are affected; however, specific cognitive impairments may differ depending on the MS subtype.
There are a number of pharmacological interventions for memory disorder in MS, including disease-modifying drugs (e.g. interferon β-1a and β-1b, glatiramer acetate, natalizumab, mitoxantrone, fingolimod, teriflunomide, dimethyl fumarate and alemtuzumab). Other therapies specific for memory disorder include acetylcholinesterase inhibitors (e.g. donepezil and rivastigmine), psychostimulants (e.g. methylphenidate, L-amphetamine sulfate, modafinil, amantadine and pemoline), N-methyl-D-aspartate antagonist (e.g. memantine) and other pharmacological agents such as Ginkgo biloba extracts, aminopyridines and cannabinoids.
Evidence that supports the use of these pharmacological agents in the treatment of memory loss in patients with MS is unclear, with inconsistencies in study results. Therefore, it is uncertain whether these pharmacological interventions are effective in treating memory disorder in MS and whether they are well tolerated to use in this population group.

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