Lou Gehrig's Disease or Amyotrophic Lateral Sclerosis (ALS) is a neurological disorder characterized by progressive degeneration of motor neuron cells in the spinal cord and brain, which ultimately results in paralysis and death. The disease takes its less-scientific name from Lou Gehrig, a baseball player with the New York Yankees in the late 1920s and 1930s, who was forced to retire in 1939 as a result of the loss of motor control caused by the disease.
In 1991, a team of researchers linked familial ALS to chromosome 21. Two years later, the SOD1 gene was identified as being associated with many cases of familial ALS. The enzyme coded for by SOD1 carries out a very important function in cells: it removes dangerous superoxide radicals by converting them into non-harmful substances. Defects in the action of this enzyme mean that the superoxide radicals attack cells from the inside, causing their death. Several different mutations in this enzyme all result in ALS, making the exact molecular cause of the disease difficult to ascertain.
Recent research has suggested that treatment with drugs called antioxidants may benefit ALS patients. However, since the molecular genetics of the disease are still unclear, a significant amount of research is still required to design other promising treatments for ALS.
In work supported by The ALS Association, researchers have shown that increasing the clearance of misfolded protein from neurons improves their survival. The study was published today in the journal Nature Chemical Biology.
Scientists at VIB and KU Leuven have demonstrated in fruit-flies that over-activity of the enzyme HDAC6 in the nerve ends exacerbates the symptoms of the neurodegenerative condition Amyotrophic Lateral Sclerosis (ALS / Lou Gehrig's Disease). Inhibition of this enzyme could offer a protective effect against ALS.
The Foundation for Mitochondrial Medicine announced today that it is working with The Michael J. Fox Foundation for Parkinson's Research to support a research project led by Wolfdieter Springer, PhD, at the Department of Neuroscience at Mayo Clinic in Florida to investigate a mitochondria-targeted therapeutic approach to treating Parkinson's disease.
Researchers believe they have learned how mutations in the gene that causes Huntington's disease kill brain cells, a finding that could open new opportunities for treating the fatal disorder. Scientists first linked the gene to the inherited disease more than 20 years ago
A selection of health policy stories from California, Maine, Massachusetts, Maryland, New Hampshire, Virginia, Iowa, Florida, Missouri, Washington state, Connecticut, Georgia, Alabama, North Carolina and Tennessee.
A team of UCLA researchers has identified a new gene involved in Parkinson's disease, a finding that may one day provide a target for a new drug to prevent and potentially even cure the debilitating neurological disorder.
When we began our Let's Move! initiative four years ago, we set one simple but ambitious goal: to end the epidemic of childhood obesity in a generation so that kids born today will grow up healthy.
It's almost axiomatic that misfolded proteins compromise how cells normally function and cause debilitating human disease, but how these proteins are detected and degraded within the body is not well understood.
Leaders from academic institutions, non-profit organizations, and pharmaceutical companies will meet in Cambridge, Mass., on Monday, May 19, to discuss biomarkers in amyotrophic lateral sclerosis (ALS).
Dr. Kerry Clark, associate professor of public health at the University of North Florida in Jacksonville, and his colleagues have found additional cases of Lyme disease in patients from several states in the southeastern U.S. These cases include two additional Lyme disease Borrelia species recently identified in patients in Florida and Georgia.
Scientists studying brain diseases may need to look beyond nerve cells and start paying attention to the star-shaped cells known as "astrocytes," because they play specialized roles in the development and maintenance of nerve circuits and may contribute to a wide range of disorders, according to a new study by UC San Francisco researchers.
A newly identified genetic disorder associated with degeneration of the central and peripheral nervous systems in humans, along with the genetic cause, is reported in the April 24, 2014 issue of Cell.
The sponginess of the environment where human embryonic stem cells are growing affects the type of specialized cells they eventually become, a University of Michigan study shows.
By studying nerve cells that originated in patients with a severe neurological disease, a University of Wisconsin-Madison researcher has pinpointed an error in protein formation that could be the root of amyotrophic lateral sclerosis.
Harvard stem cell scientists have discovered that a recently approved medication for epilepsy may possibly be a meaningful treatment for amyotrophic lateral sclerosis (ALS)-Lou Gehrig's disease, a uniformly fatal neurodegenerative disorder. The researchers are now collaborating with Massachusetts General Hospital to design an initial clinical trial testing the safety of the treatment in ALS patients.
The Cedars-Sinai Regenerative Medicine Institute has received a $2.5 million grant from the Department of Defense to conduct animal studies that, if successful, could provide the basis for a clinical trial of a gene therapy product for patients with Lou Gehrig's disease, also called amyotrophic lateral sclerosis, or ALS.
In work supported by The ALS Association, researchers have discovered a new ALS-causing gene and have linked its function to that of another prominent disease gene. The study was published in the journal Nature Neuroscience.
Amyotrophic lateral sclerosis, also known as Lou Gehrig's disease, is marked by a cascade of cellular and inflammatory events that weakens and kills vital motor neurons in the brain and spinal cord. The process is complex, involving cells that ordinarily protect the neurons from harm. Now, a new study by scientists in The Research Institute at Nationwide Children's Hospital points to a potential culprit in this good-cell-gone-bad scenario, a key step toward the ultimate goal of developing a treatment.
As stem cells continue their gradual transition from the lab to the clinic, a research group at the University of Wisconsin-Madison has discovered a new way to make large concentrations of skeletal muscle cells and muscle progenitors from human stem cells.
Neuralstem, Inc. (NYSE MKT: CUR) announced that the final results from the Phase I safety trial using NSI-566 spinal cord stem cells in the treatment of amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease) were published in the peer-reviewed journal, "Annals of Neurology".
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