Recent advances in stem cell biology have raised expectations that both diseases of, and injuries to, the central nervous system may be ameliorated by cell transplantation. In particular, cell therapy has been studied for inducing efficient remyelination in disorders of myelin, including both the largely pediatric disorders of myelin formation and maintenance and the acquired demyelinations of both children and adults. Potential cell-based treatments of two major groups of disorders include both delivery of myelinogenic replacements and mobilization of residual oligodendrocyte progenitor cells as a means of stimulating endogenous repair; the choice of modality is then predicated upon the disease target. In this review we consider the potential application of cell-based therapeutic strategies to disorders of myelin, highlighting the promises as well as the problems and potential perils of this treatment approach.
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http://dx.doi.org/10.1196/annals.1444.014 | DOI Listing |
World J Stem Cells
January 2025
First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300381, China.
Peripheral nerve injury (PNI) is a common disease that is difficult to nerve regeneration with current therapies. Fortunately, Zou demonstrated the role and mechanism of bone marrow derived mesenchymal stem cells (BMSCs) in promoting nerve regeneration, revealing broad prospects for BMSCs transplantation in alleviating PNI. We confirmed the fact that BMSCs significantly alleviate PNI, but there are shortcomings such as low cell survival rate and immune rejection, which limit the wide application of BMSCs.
View Article and Find Full Text PDFHeliyon
January 2025
Center for Brain Immunology and Glia, Department of Neuroscience, Charlottesville, VA 22908, USA.
Background: Variants in the gene have been identified as a risk factor for late-onset Alzheimer's disease and are linked to decreased white matter integrity in healthy adults. However, the specific role for clusterin in myelin maintenance in the context of Alzheimer's disease remains unclear.
Methods: We employed a combination of immunofluorescence and transmission electron microscopy techniques, primary culture of OPCs, and an animal model of Alzheimer's disease.
Ann Indian Acad Neurol
January 2025
Centre for Advanced Neurological Research, KS Hegde Medical Academy, Nitte University, Mangalore, Karnataka, India.
Myelin oligodendrocyte glycoprotein antibody-associated disease has been recently identified to be a distinct autoimmune central nervous system disorder. There is significant clinical and radiological overlap with multiple sclerosis and aquaporin-4-IgG-associated neuromyelitis optica spectrum disorders. Clinical course is variable in that patients may have a monophasic or relapsing course, disease severity is unpredictable, and unlike other idiopathic autoimmune inflammatory disorders, there is no gender predilection and it is more likely to affect pediatric population.
View Article and Find Full Text PDFJ Biol Chem
January 2025
Department of Neurology, Henry Ford Health, Detroit, MI 48202, USA. Electronic address:
Multiple sclerosis (MS) is a prevalent inflammatory neurodegenerative disease in young people, causing neurological abnormalities and impairment. To investigate a novel therapeutic agent for MS, we observed the impact of maresin 1 (MaR1) on disease progression in a well-known, relapsing-remitting experimental autoimmune encephalomyelitis (RR-EAE) mouse model. Treatment with MaR1 accelerated inflammation resolution, reduced neurological impairment, and delayed disease development by reducing immune cell infiltration (CD4+IL-17+ and CD4+IFNγ+) into the central nervous system (CNS).
View Article and Find Full Text PDFMult Scler
January 2025
Department of Neurology, Mayo Clinic, Rochester, MN, USA.
Testing for myelin oligodendrocyte glycoprotein immunoglobulin G antibodies (MOG-IgG) is essential to the diagnosis of MOG antibody-associated disease (MOGAD). Due to its central role in the evaluation of suspected inflammatory demyelinating disease, the last 5 years has been marked by an abundance of research into MOG-IgG testing ranging from appropriate patient selection, to assay performance, to utility of serum titers as well as cerebrospinal fluid (CSF) testing. In this review, we synthesize current knowledge pertaining to the "who, what, where, when, why, and how" of MOG-IgG testing, with the aim of facilitating accurate MOGAD diagnosis in clinical practice.
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