A study finds that overexpression of the macrophage migration inhibitory factor, or MIF, in the spinal cords of mice with mutations in superoxide dismutase (SOD1), an enzyme associated with protein misfolding and amyotrophic lateral sclerosis (ALS), suppressed the misfolding and aggregation of SOD1, delaying disease onset and extending the lifespan of mice with the mutation; the results suggest a potential therapeutic role for MIF in ALS, according to the authors.
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Article #19-04665: "AAV2/9-mediated overexpression of MIF inhibits SOD1 misfolding, delays disease onset, and extends survival in mouse models of ALS," by Marcel F. Leyton-Jaimes, Joy Kahn, and Adrian Israelson.
MEDIA CONTACT: Adrian Israelson, Ben-Gurion University of the Negev, Beer Sheva, ISRAEL; e-mail: <adriani@bgu.ac.il>
Journal
Proceedings of the National Academy of Sciences