News Release

Delaying ALS onset in mice

Peer-Reviewed Publication

Proceedings of the National Academy of Sciences

Spinal cord of mutant SOD1 mouse showing motor neurons in green and activated microglia in red.

image: Spinal cord of mutant SOD1 mouse showing motor neurons in green and activated microglia in red. view more 

Credit: Image courtesy of Marcel F. Leyton-Jaimes.

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>


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