Multiple sclerosis (MS) is an autoimmune condition that causes inflammatory damage to the central nervous system. The pathologic features are diffuse and focal inflammation, demyelination, gliosis, and neuronal damage in the optic nerves, brain, and spinal cord. Multiple sclerosis remains a challenging and disabling disease. There is a greater understanding of the underlying genetic and environmental factors driving the disorder, including low vitamin D levels, smoking, and obesity. Early and accurate diagnosis is essential and needs to be supported by diagnostic criteria, including imaging and spinal fluid abnormalities in patients with clinically isolated syndromes. Other demyelinating diseases are neuromyelitis optica spectrum disorders (NMOSD), anti-myelin oligodendrocyte glycoprotein antibody disease (MOGAD), and acute disseminated encephalomyelitis (ADEM).
MS remains an incurable disease, and although some conventional treatments and even targeted therapies can improve symptoms and reduce the number and severity of relapses, these failed to control disease progression. In recent years, some parallel pathophysiological mechanisms in the pathogenesis of MS have been elucidated, including oligodendrocytes dysfunction, blood-brain barrier abnormalities, metabolic alterations, and immunosenescence. These findings provide new potential biomarkers at disease onset, early during the disease course, and treatment response for MS. Due to the lack of a classic animal model, some of the pathogenesis of NMOSD remains unclear, especially seronegative NMOSD. The titers of AQP4-IgG and MOG-IgG are not wholly relevant to relapse risk or disease severity. Therefore, it is necessary to explore more valuable predictors. Furthermore, it is the diagnostic dilemma between NMOSD and MOGAD when autoimmune antibodies have low serum levels of coexisting or negative antibodies. Thus, there are emerging challenges in understanding the pathogenesis and developing diagnostic and therapeutic strategies.
This Research Topic aims to provide recent advances and novel findings on mechanisms, biomarkers, and therapeutic targets for MS and related diseases, including NMOSD and MOGAD. We welcome Original Research, Reviews, Editorials, Commentaries, and Perspective submissions. Topics of interest include but are not limited to:
- Molecular mechanisms and signaling pathways in the pathogenesis of MS and related diseases;
- The genetic, epigenetic, and transcriptomic factors in MS and related diseases;
- Innovative serum biomarkers and prognostic factors in MS and related diseases;
- Comparison of autoimmunity between MS and other related diseases like NMOSD, MOGAD, ADEM, and autoimmune glial fibrillary acidic protein(GFAP) astrocytopathy;
- Immunosenescence and Immunometabolism in MS and related diseases;
- The potential therapeutic approaches for MS and related diseases.
Multiple sclerosis (MS) is an autoimmune condition that causes inflammatory damage to the central nervous system. The pathologic features are diffuse and focal inflammation, demyelination, gliosis, and neuronal damage in the optic nerves, brain, and spinal cord. Multiple sclerosis remains a challenging and disabling disease. There is a greater understanding of the underlying genetic and environmental factors driving the disorder, including low vitamin D levels, smoking, and obesity. Early and accurate diagnosis is essential and needs to be supported by diagnostic criteria, including imaging and spinal fluid abnormalities in patients with clinically isolated syndromes. Other demyelinating diseases are neuromyelitis optica spectrum disorders (NMOSD), anti-myelin oligodendrocyte glycoprotein antibody disease (MOGAD), and acute disseminated encephalomyelitis (ADEM).
MS remains an incurable disease, and although some conventional treatments and even targeted therapies can improve symptoms and reduce the number and severity of relapses, these failed to control disease progression. In recent years, some parallel pathophysiological mechanisms in the pathogenesis of MS have been elucidated, including oligodendrocytes dysfunction, blood-brain barrier abnormalities, metabolic alterations, and immunosenescence. These findings provide new potential biomarkers at disease onset, early during the disease course, and treatment response for MS. Due to the lack of a classic animal model, some of the pathogenesis of NMOSD remains unclear, especially seronegative NMOSD. The titers of AQP4-IgG and MOG-IgG are not wholly relevant to relapse risk or disease severity. Therefore, it is necessary to explore more valuable predictors. Furthermore, it is the diagnostic dilemma between NMOSD and MOGAD when autoimmune antibodies have low serum levels of coexisting or negative antibodies. Thus, there are emerging challenges in understanding the pathogenesis and developing diagnostic and therapeutic strategies.
This Research Topic aims to provide recent advances and novel findings on mechanisms, biomarkers, and therapeutic targets for MS and related diseases, including NMOSD and MOGAD. We welcome Original Research, Reviews, Editorials, Commentaries, and Perspective submissions. Topics of interest include but are not limited to:
- Molecular mechanisms and signaling pathways in the pathogenesis of MS and related diseases;
- The genetic, epigenetic, and transcriptomic factors in MS and related diseases;
- Innovative serum biomarkers and prognostic factors in MS and related diseases;
- Comparison of autoimmunity between MS and other related diseases like NMOSD, MOGAD, ADEM, and autoimmune glial fibrillary acidic protein(GFAP) astrocytopathy;
- Immunosenescence and Immunometabolism in MS and related diseases;
- The potential therapeutic approaches for MS and related diseases.
