Abstract
Multiple sclerosis (MS) is a demyelinating, autoimmune disease of the central nervous system. In recent years, it has become more evident that neurodegeneration, including neuronal damage and axonal injury, underlies permanent disability in MS. This manuscript reviews some of the mechanisms that could be responsible for neurodegeneration and axonal damage in MS and highlights the potential role that dysfunctional heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) and antibodies to hnRNP A1 may play in MS pathogenesis.
Highlights
Contribution of the Degeneration of theSalapa 1 , Sangmin Lee 2,3 , Yoojin Shin 2,3 and Michael C
Because antibodies to other non-myelin antigens, such as neurofascin, have been shown to worsen EAE and lead to axonal damage, we hypothesized that anti-hnRNP A1-M9 antibodies, which recognize the same immunodominant epitope as Multiple sclerosis (MS) patient IgG, might show similar effects
By using RNA immunoprecipitation, we found that SP4 and SPG7 bound hnRNP A1 while SPG20 did not [3,66]
Summary
Salapa 1 , Sangmin Lee 2,3 , Yoojin Shin 2,3 and Michael C.
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