ST. PAUL, Minn. – New guidelines from the American Academy of Neurology identify the most effective treatments for amyotrophic lateral...
Research into amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, has lead to new information about neuronal loss...
Researchers discover common cause of all forms of ALS. The underlying disease process of amyotrophic lateral sclerosis (ALS and Lou Gehrig’s disease), a fatal neurodegenerative disease that paralyzes its victims, has long eluded scientists and prevented development of effective therapies. Scientists weren’t even sure all its forms actually converged into a common disease process.
Researchers from the Bellvitge Biomedical Research Institute at the University of Barcelona have coordinated research into how the IDPN nitrile causes neurological syndromes similar to those of the amyotrophic lateral sclerosis (ALS), a severe neuromuscular degenerative disease.
Scientists knew that mutations in the FUS gene (Fused in Sarcoma) cause amyotrophic lateral sclerosis (ALS), a disease of the nerve cells in the brain and spinal cord that control voluntary muscle movement. The researchers were successful in identifying mutations in this gene that cause Essential Tremor, and proved that the disease mechanisms for ET and ALS FUS mutations are different.
By increasing the signaling activity of a protein called muscle skeletal receptor tyrosine-protein kinase (MuSK), researchers were able to keep nerve cells attached to muscle longer into the progression of the disease in a mouse model of ALS.
Professional football players in this study were three times more likely to die as a result of diseases that damage brain cells compared to the general population. A player’s risk of death from Alzheimer’s disease or ALS was almost four times higher than the general population.
Efforts to treat disorders like Lou Gehrig’s disease, Paget’s disease, inclusion body myopathy and dementia will receive a considerable boost from a new research model created by UC Irvine scientists.
Researchers have identified a new genetic mutation for amyotrophic lateral sclerosis (ALS), opening the door to future targeted therapies.
A new finding turns one of the basics of neurobiology on its head, demonstrating that it is possible to turn one type of already differentiated neuron into another within the brain.
While evidence suggests pathological proteins linked to the onset and progression of neurodegenerative disorders are capable of spreading from cell-to-cell within the brains of affected individuals, new research shows no evidence to support concerns that these abnormal disease proteins are “infectious” or transmitted from animals to humans or from one person to another.
Researchers discover an abnormal protein that accumulates in the brains of patients affected with ALS and frontotemporal dementia. The findings have uncovered a potentially new therapeutic target and biomarker that would allow clinicians to confirm diagnosis of the diseases.
