“There hasn’t been a lot of ambiguity in Art’s lab as to what the mission has been,” says Lifton. “In whatever direction the project needs him to go to become expert, he does that. It’s one of the hallmarks of a great scientist, following the trail wherever it leads.”

But beyond elucidating the basic biology of ALS, Horwich is not shy about his ultimate goal. “If, when my children’s tennis coach first started limping we had known what to do to arrest the process associated with aggregation of these proteins, he would still be alive,” he says. “That would be the dream.”

To that end, Horwich has treated some of his mutant mice with experimental therapies; in others, he is investigating how variations in the SOD1 gene affect the progression of disease. He is also exploring whether it’s possible to get cells to ramp up their production of chaperone proteins, amplifying their ability to capture free-floating unfolded proteins that might otherwise clump together.

It’s too soon to say whether any of these approaches will yield a viable treatment. For Horwich, who in the GroEL days grew accustomed to experiments that could be conceived and completed in a single day, the work is maddeningly slow. Still, his characteristic optimism is on full display.

“I keep going in the mouse room and hoping that we will be able to see an animal whose disease improves because of something we can track,” he says. But “whether we’re successful at trying this huge thing that we’re trying to tackle or not, I’m still going to come to work. I’m still going to tinker side by side with my group.”

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