Ben-Gurion U. study highlights gene that could lead to therapies for ALS

For the first time, this study reported that ‘endogenous multifunctional protein macrophage migration inhibitory factor (MIF),’ a gene that regulates cell inflammation and immunity, acts as a chaperone for misfolded SOD1 in a mouse model. The researchers demonstrated that completely eliminating MIF in a mutant SOD1 mouse model of familial ALS increased misfolded SOD1 accumulation. This also accelerated disease onset and late disease progression and shortened the lifespan of mice expressing mutant SOD1.
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