Abstract
Neurodegeneration in multiple sclerosis (MS) is believed to underlie disease progression and permanent disability. Many mechanisms of neurodegeneration in MS have been proposed, such as mitochondrial dysfunction, oxidative stress, neuroinflammation, and RNA-binding protein dysfunction. The purpose of this review is to highlight mechanisms of neurodegeneration in MS and its models, with a focus on RNA-binding protein dysfunction. Studying RNA-binding protein dysfunction addresses a gap in our understanding of the pathogenesis of MS, which will allow for novel therapies to be generated to attenuate neurodegeneration before irreversible central nervous system damage occurs.
Highlights
Neurodegeneration is a frequently used term to describe many neurological diseases, but its precise definition varies
This review focuses on mechanisms of neurodegeneration resulting from mitochondrial dysfunction, oxidative stress, and neuroinflammation, and provides a summary of data suggesting that dysfunctional RNA-binding proteins may contribute to multiple sclerosis (MS) pathogenesis of neurodegeneration in MS
While all IgG are capable of binding Fc receptors, we have shown that compared to anti-hnRNP A1 antibodies, isotype control IgG did not localize to the spinal cord and did not colocalize with Fc receptors on macrophages [70,134]
Summary
Neurodegeneration is a frequently used term to describe many neurological diseases, but its precise definition varies. Neurodegeneration is the breakdown of the nervous system, a very broad understanding of the term that is open to interpretation. It may be defined as the death or damage to cells of the nervous system which may include neurons, oligodendrocytes, and other glial cells. In this review neurodegeneration is defined as the death and damage to central nervous system (CNS) neuronal cell bodies and their axons. In diseases with a neurodegenerative component, the death of neurons is not usually the direct cause of mortality, but rather facilitates the occurrence of secondary health problems [1]. This review provides the most current knowledge and gaps in our understanding of the mechanisms underlying neurodegenerative processes occurring in MS and its models
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