News

Scientists identify mutation in SIGMAR1 gene linked to juvenile amyotrophic lateral sclerosis
Aug 12, 2011
Researchers from the Kingdom of Saudi Arabia have identified a mutation on the SIGMAR1 gene associated with the development of juvenile amyotrophic lateral sclerosis. Study findings published today in Annals of Neurology show the gene variant affects Sigma-1 receptors which are involved in motor neuron function and disease development.
New model of amyotrophic lateral sclerosis is based on human cells from autopsied tissue
Aug 11, 2011
By isolating cells from patients' spinal tissue within a few days after death, researchers have developed a new model of amyotrophic lateral sclerosis. They found that during the disease, cells called astrocytes become toxic to nerve cells – a result previously found in animal models but not in humans.
Scientists solve mystery of nerve disease genes
Jul 05, 2011
For several years, scientists have been pondering a question about a genetic disease called Charcot-Marie-Tooth (CMT) disease type 2D: how can different types of mutations, spread out across a gene, produce the same condition? The findings of a new study may also have implications for other diseases, such as amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig disease.
Stem cell model offers clues to cause of inherited amyotrophic lateral sclerosis
Jun 22, 2011
An international team of scientists led by researchers at the University of California, San Diego School of Medicine have used induced pluripotent stem cells (iPSCs) derived from patients with amyotrophic lateral sclerosis to reveal for the first time how reduced levels of a specific protein may play a central role in causing at least 1 inherited form of the disease.
Connection discovered between the nervous system and the vascular system
Jun 08, 2011
Researchers have shown for the first time that a key molecule of the vascular system directs axons during the formation of neural circuits. This connection between the nervous system and the vascular system could be a good starting point for the development of therapies for neurodegenerative diseases.
Mild obesity appears to improve survival in amyotrophic lateral sclerosis patients
May 12, 2011
In a retrospective study of over 400 amyotrophic lateral sclerosis patients, Massachusetts General Hospital researchers found that those who were mildly obese survived longer than patients who were normal weight, underweight, or even overweight.
Researchers make strides in understanding amyotrophic lateral sclerosis
Apr 26, 2011
Brandeis researchers have made a significant advance in the effort to understand amyotrophic lateral sclerosis (ALS) by successfully reversing the toxicity of the mutated protein in the familial type of the disease.
Research discovery may block amyotrophic lateral sclerosis disease process
Apr 19, 2011
In the first animal model of amyotrophic lateral sclerosis, a LSU Health Sciences Center New Orleans lab has found that blocking the abnormal movement of a protein made by a mutated gene called FUS also blocks the disease process.
New study suggests amyotrophic lateral sclerosis could be caused by a retrovirus
Mar 02, 2011
A retrovirus that inserted itself into the human genome thousands of years ago may be responsible for some cases of the neurodegenerative disease amyotrophic lateral sclerosis. The finding, made by Johns Hopkins scientists, may eventually give researchers a new way to attack this universally fatal condition.
Cigarette smoking associated with increased risk of developing amyotrophic lateral sclerosis
Feb 17, 2011
Rates of amyotrophic lateral sclerosis increased with age and were higher in men in all age groups, and those who had ever smoked cigarettes at the beginning of the study had an increased risk of amyotrophic lateral sclerosis compared with those who had never smoked.
Malfunctioning gene associated with amyotrophic lateral sclerosis leads to neuron death in mice
Jan 05, 2011
Amyotrophic lateral sclerosis (ALS), and frontotemporal lobar degeneration (FTLD) are characterized by protein clumps in brain and spinal-cord cells that include an RNA-binding protein called TDP-43. This protein is the major building block of the lesions formed by these clumps. A study published in the Journal of Clinical Investigation describes the first direct evidence of how mutated TDP-43 can cause neurons to die.