The MIT biologist studies how RNA molecules self-assemble and the role these accumulations may play in diseases such as ALS and Huntington’s.

The group’s 7-2 ruling in favor of the therapeutic represents a shift from previous deliberations, in which data on its effectiveness was deemed insufficient.

The country’s provisional go-ahead could increase pressure already being exerted on the US Food and Drug Administration to approve the therapy.

The patient, who has ALS, is able to communicate in complete sentences by deliberately altering his brain’s activity.

The long noncoding RNA MINCR, implicated in ALS and Alzheimer’s disease as well as several types of cancer, appears to function differently when present at high versus low levels.

Conservation of structures and functions between single-celled fungi and human cells allow researchers to probe the brain.

Meet some of the people featured in the October 2021 issue of The Scientist.

The single-celled fungus allows researchers to study Alzheimer’s, Parkinson’s, ALS and other brain diseases with unparalleled speed and scale.

After six months, patients with fast-progressing amyotrophic lateral sclerosis who had received the experimental treatment had less loss of function than those who received a placebo.

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.