Remyelinating and neuroprotective treatments in multiple sclerosis

Stangel, Martin

doi:10.1517/13543784.13.4.331

Cited by 22Multiple Sclerosis Research StudiesSpinal Cord Injury ResearchNeurogenesis and neuroplasticity mechanisms

Remyelinating and neuroprotective treatments in multiple sclerosis

Stangel, Martin·2004·Expert Opinion on Investigational Drugs

DOI 10.1517/13543784.13.4.331

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Abstract

Multiple sclerosis (MS) is the most common cause of neurological disability in young adults. The pathological hallmark is multifocal demyelination and inflammation in the CNS. In addition, there is also a variable extent of axonal damage. Remyelination has been seen in up to 70% of lesions but repair is generally incomplete. The demonstration of neuropathological heterogeneity of MS lesions suggests different pathophysiological subtypes and it is therefore unlikely that there is a uniform cause of incomplete remyelination in MS. In recent years, a great body of knowledge has accumulated in order to better understand the regulatory mechanisms of remyelination. This has led to a number of approaches to promote repair mechanisms, most of which have been successful in animal experiments. Unfortunately, the translation of these experimental data into clinical treatments has proven difficult. More information on the pathogenesis of MS, the reason why repair mechanisms fail in MS and a better understanding of the regulation of remyelination are required. This will ultimately lead to a specific treatment tailored for the individual patient and will probably involve a combination of immunomodulation, remyelination and neuroprotection.

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Variable conduction delays might lead to unpredictable variations in synaptic strength, such as have previously been suggested to underlie corollary discharge abnormalities in schizophrenia.
“Furthermore, given the role that spike-timing dependent plasticity has been proposed to play in efference copy circuits, 78 variable conduction delays might also lead to unpredictable variations in synaptic strength, such as have previously been suggested to underlie corollary discharge abnormalities in patients with schizophrenia.78”
From Schizophrenia, myelination, and delayed corollary discharges: a hypothesis (2012) · cites this paper as [78]

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Authors: Stangel, M.
Affiliations: Medizinische Hochschule Hannover (DE)
Corresponding author: Stangel, Martin
ORCID: Stangel, Martin
Venue: Expert Opinion on Investigational Drugs
Publisher: Informa Healthcare
Published: 2004-04
Volume: 13
Issue: 4
Pages: 331-347
ISSN: 1354-3784 (ISSN-L)
1744-7658
DOI: 10.1517/13543784.13.4.331
OpenAlex: W2096544375
Cited by: 22
References: 211
Citations by year: 2025: 1 · 2022: 1 · 2020: 1 · 2018: 1 · 2014: 1 · 2013: 1
FWCI: 0.23
Type: journal article
Language: en
Open access: closed
Locations: Expert Opinion on Investigational Drugs (publishedVersion)
PubMed (publishedVersion)
Funders: Deutsche Forschungsgemeinschaft
Topics: Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
Health Sciences › Medicine › Pathology and Forensic Medicine › Spinal Cord Injury Research
Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords: multiple sclerosis, remyelination, neuroprotection, demyelination, axonal injury, immunomodulation, clinical translation
MeSH terms: Animals, Humans, Multiple Sclerosis, Nerve Fibers, Myelinated, Neuroprotective Agents

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Remyelinating and neuroprotective treatments in multiple sclerosis

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