Mice born with Spinal Muscular Atrophy typically only live five to six days. University of Missouri researchers introduced the SMN gene into the mice’s central nervous systems and were able to extend their lives 10-25 days longer.
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A study suggests that spinal muscular atrophy (SMA), a genetic neuromuscular disease in infants and children, results primarily from motor circuit dysfunction, not motor neuron or muscle cell dysfunction, as is commonly thought. In a second study, the researchers identified the molecular pathway in SMA that leads to problems with motor function.
Researchers identify Neurexin2 as a new target for potential treatment of spinal muscular atrophy.
A new study uncovers molecular changes which may explain why motor neurons, rather than other neurons, are affected by the childhood illness, SMA.
Researchers report insufficient blood supply could contribute to motor neuron loss in SMA.
A new study implicates a key cellular mechanism as defective in SMA for the first time, providing a new lead for developing future interventions.
A new drug shows promise for improving outcomes for people with SMA.
Researchers believe they have discovered a promising new treatment for spinal muscular atrophy, a leading genetic cause of death in children.
Researchers have identified a compound that can stabilize a protein implicated in ALS and SMN.
Researchers implicate a variant in the UBQLN4 gene as a possible cause of ALS. The variant disrupts cellular processes that drive motor neuron development.
WUSTL researchers have converted skin cells into motor neurons without going through the stem cell state. The new technique could help in the development of devastating neurodegenerative diseases, like ALS, that affect motor neurons.
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Targeting autophagy may help in the battle against ALS and other diseases that affect motor neurons, researchers report.