Antibody Binds to Movement
Memory B-cell antibody targets misfolded SOD1. Treatment with α-miSOD1 ameliorates ALS motor symptoms.
Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disease that affects motor neurons by biological mechanisms such as misfolded protein aggregation, which causes neuronal death. Lower and upper motor neurons allow the signaling of voluntary movement from the nervous system to the muscles (Taylor et al. 2016). There is not a clear cause for ALS as 90% of all patients are considered sporadic (SALS), which means there is no inherited gene mutation. Nevertheless, research on familial ALS (FALS) has allowed the identification of over 50 genes related to ALS: C9ORF72, FUS (fused in sarcoma), TDP-42 (TAR-DNA binding protein) and SOD1 (superoxide dismutase 1), among others (Mejzini et al. 2019). SOD1 is an enzyme that has a key role in the detoxification of superoxide anion radicals in the cell and when this gene is mutated, misfolding creates toxic inclusions and aggregation (Mejzini et al. 2019). Writing in Science Translational Medicine, Maier et al. (2018), explore the possibility of an immunological response triggered by misfolded SOD1 that generates neo-epitopes and B cell memory alongside with the possible use of it for immunotherapy.