Researchers Have Discovered a Mechanism Underlying ALS

A study has discovered a mechanism involved in amyotrophic lateral sclerosis (ALS). The researchers hope that this new information could contribute to finding a treatment for the condition. The full article is available here, at Tel Aviv University website.

ALS is a condition that affects the brain and nerves and causes progressive weakness. It is a type of motor neurone disease that breaks down motor neurone cells in the brain, spinal cord, and muscles that are involved in voluntary movement. This cell degeneration can prevent the brain from effectively sending messages to the muscles, resulting in a loss of motor, or movement, control. Over time, the muscles weaken and atrophy. Approximately 15,000 people in the US are estimated to have ALS, and it is the most common neuromuscular disease.

However, some of the underlying mechanisms behind ALS remain poorly understood. Researchers have recently linked altered microRNAs to ALS and many other neurodegenerative diseases. MicroRNAs are molecules involved in regulating gene expression. The recent study, published in the Journal of Neuroscience, builds on this information.
It outlines a mechanism linked to ALS that involves the muscles secreting molecules that are toxic and kill parts of nerve cells that conduct messages (axons) and the link between motor neurones and muscle fibres (neuromuscular junctions), and is therefore thought to lead to muscular atrophy. Furthermore, the microRNA 126-5p was linked to increased levels of toxic molecules in pre-symptomatic ALS mouse models.
The researchers then used this information to increase the expression of microRNA 126-5p in lab work and mouse models and found that this affected ALS symptoms. In mice, manipulating microRNA 126-5p led to improvement in the ability to walk, neuromuscular function, and muscle atrophy.
Researchers are hopeful that these findings could contribute to the development of a treatment for ALS. The team is now planning to carry out another study into non-muscular tissues damaged by ALS.