Molecular Research on Pathophysiology of Multiple Sclerosis and Neuroinflammation
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".
Deadline for manuscript submissions: 20 January 2025 | Viewed by 78
Special Issue Editor
Interests: neurodegeneration; neuroinflammation; multiple sclerosis; amyotrophic lateral sclerosis; animal models of neural diseases; neural biomarkers; calcium-binding neuroproteins; S100B protein
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS). Inflammatory demyelination of white matter in the CNS, characterized by acute phases alternating remission phases, is the main pathological feature of MS and of experimental autoimmune encephalomyelitis, which is its animal model equivalent, regarded as reliable. A distinctive feature of inflammatory demyelination is the complex coordination of innate and adaptive immune processes. Recovery from nerve damage and degeneration after neuroinflammation at present is very difficult, probably owing to a lack of effective remedies. Thus, a better comprehension of the physiopathological processes underlying neuroinflammation during the different phases characterizing MS would help us to understand the disease and, as a result, identify efficacious therapeutic targets and, in any case, therapeutic strategies useful to counteract the disease.
The present Special Issue aims to collate original contributions and reviews exploring pathways that will lead us to the above goal. Both experimental pre-clinical studies and clinical studies involving patients will be considered, including those investigating the use of biomarkers.
Prof. Dr. Fabrizio Michetti
Guest Editor
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Keywords
- multiple sclerosis (MS)
- autoimmune diseases
- encephalomyelitis
- neuroinflammation
- central nervous system (CNS)
- autoimmunity and neurodegeneration
- molecular basis of immune mechanisms
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