Mechanisms of Neurodegeneration in Multiple Sclerosis

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS), which leads to the formation of foci of primary demyelination in the white and gray matter and diffuse damage to axons and neurons. Despite significant progress in the development of drugs for relapsing-re...

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Vydáno v:Neuroscience and behavioral physiology Ročník 53; číslo 3; s. 324 - 332
Hlavní autoři: Eliseeva, D. D., Zakharova, M. N.
Médium: Journal Article
Jazyk:angličtina
Vydáno: Cham Springer International Publishing 01.03.2023
Springer Nature B.V
Témata:
Axons
Behavioral Sciences
Biomedical and Life Sciences
Biomedicine
Blood-brain barrier
Central nervous system
Demyelination
Drug development
Glycoproteins
Hypoxia
Inflammatory diseases
Lymphocytes
Macrophages
Medical research
Microglia
Multiple sclerosis
Myelination
Nervous system
Neurobiology
Neurodegeneration
Neurons
Neurosciences
Oligodendrocytes
Oxidative stress
Substantia grisea
progression of disability
neurodegeneration
multiple sclerosis
demyelination
ISSN:0097-0549, 1573-899X
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Popis
Shrnutí:Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS), which leads to the formation of foci of primary demyelination in the white and gray matter and diffuse damage to axons and neurons. Despite significant progress in the development of drugs for relapsing-remitting MS, the impact on the progression of the disease remains insufficient. Diffuse and compartmentalized lymphocyte and macrophage infiltration of CNS tissue inhibits the differentiation of myelinating mature oligodendrocytes and disrupts remyelination processes. Chronic inflammation, which occurs when the blood–brain barrier (BBB) is intact, activates microglia, increasing axon and neuron damage and, as a result, triggers chronic oxidative stress and histotoxic hypoxia. It is currently important to clarify the mechanisms underlying neurodegeneration, which in the later stages of MS is caused by chronic neuroaxonal damage and impairment of regenerative capabilities and which largely determines disease outcome.
Bibliografie:ObjectType-Article-1
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ISSN:0097-0549
1573-899X
DOI:10.1007/s11055-023-01429-1