Researchers identify new motor neuron subgroups and gain insights into amyotrophic lateral sclerosis (ALS).

Researchers slowed disease progression in the mice by injecting two different viral vectors, each containing one part of the DNA encoding the Cas9 protein, to edit the causative gene.

Flexible proteins appear to protect molecules from becoming denatured in extreme conditions such as heat and from clumping up, as happens in some neurodegenerative diseases.

Boosting the levels of Akkermansia muciniphila in mouse guts slowed the progression of an ALS-like disease, while two other microbiome members were associated with more severe symptoms.

He developed an MRI-based map of the human cortex, discovered genetic risk factors for neurodegenerative diseases, and wrote about his struggles with ALS.

Famed for his work on black holes and cosmology, he also survived decades with amyotrophic lateral sclerosis.

The gene-editing tool was effective in disabling a defective gene responsible for some forms of amyotrophic lateral sclerosis. 

By stifling autophagy in the motor neurons of a mouse model of amyotrophic lateral sclerosis (ALS), scientists stem later-stage disease progression.

Amyotrophic lateral sclerosis patients in the U.S. now have an option besides riluzole, which was approved by the FDA more than two decades ago and only extends life by two or three months.