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 a study that demonstrates the promise of cell-based therapies for diseases that have proved intractable to modern medicine, a team of scientists from the University of Wisconsin-Madison has shown it is possible to rescue the dying neurons characteristic of amyotrophic lateral sclerosis (ALS), a fatal neuromuscular disorder also known as Lou Gehrig's disease.
Chemists from UCLA and the University of Florence in Italy may have solved an important mystery about a protein that plays a key role in a particular form of amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, a progressive, fatal neurodegenerative disorder that strikes without warning.
Moderate strengthening exercises may help people with early stage ALS maintain function and quality of life longer, according to a study published in the June 5, 2007, issue of Neurology, the scientific journal of the American Academy of Neurology.
University of Kentucky researchers have discovered a new cellular mechanism that may better explain what causes amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's Disease.
A small pilot study suggests that testosterone treatment is safe, well tolerated and may reduce symptoms, slow brain degeneration and increase muscle mass in men with relapsing-remitting multiple sclerosis, the most common form of the disease, according to a report in the May issue of Archives of Neurology, one of the JAMA/Archives journals.
Researchers at the University of Toronto's Faculty of Medicine have developed the first antibody that detects the only known cause of amyotrophic lateral sclerosis (ALS), also called Lou Gehrig's disease.
Most research on Lou Gehrig's disease therapeutics has been based on the assumption that its two forms (sporadic and hereditary) are similar in their underlying cause.
Researchers from The Ludwig Institute and the University of California, San Diego (UCSD) School of Medicine have discovered that when motor neurons damaged by amyotrophic lateral sclerosis (ALS), or Lou Gehrig?s disease, inappropriately send the wrong signal, immune cells react by killing the messenger.
Avicena Group has announced that it has filed a composition of matter patent application with the United States Patent and Trademark Office for Amyotrophic Lateral Sclerosis (ALS, or Lou Gehrig's disease), a severe neurodegenerative disease.
Results of two studies funded by Project A.L.S. and appearing in the advance online publication of Nature Neuroscience demonstrate that embryonic stem cells may provide a new tool for studying disease mechanisms and for identifying drugs to slow ALS, also known as Lou Gehrig's disease.
An estimated 5,600 people in the United States are diagnosed every year with Amyotrophic Lateral Sclerosis (ALS), also known as Lou Gehrig's disease, and as many as 30,000 Americans have the disease at any given time.
Two papers by Columbia and Harvard researchers report for the first time that astrocytes (the most abundant non-neuronal cells in the central nervous system), which carry a mutated gene known to cause some cases of amyotrophic lateral sclerosis (ALS/Lou Gehrig's disease), induce motor neuron death.
For the millions of Americans whose vision is slowly ebbing due to degenerative diseases of the eye, the lowly neural progenitor cell may be riding to the rescue.
Whether a supplement used by athletes to boost energy levels and build muscle can slow progression of Parkinson's disease is the focus of a North American study.
Scientists who focus on the molecular signaling that underlies prostate cancer have discovered a compound that shows promise against a debilitating neurodegenerative condition known as Kennedy's disease, which is caused by a mutant gene.
Sufferers from devastating neurodegenerative diseases have been given some hope by the results of recent research.
In the first genome-wide search for the genetic roots of the most common form of amyotrophic lateral sclerosis (ALS), Johns Hopkins scientists have newly identified 34 unique variations in the human genetic code among 276 unrelated subjects with ALS.
A new review of hundreds of research articles has shown that the prevalence of multiple sclerosis (MS) is far higher than previously thought amongst the U.S. population.
According to the Journal, the number of young people caring for parents with debilitating conditions -- such as Lou Gehrig's disease, multiple sclerosis, lupus, cancer and heart disease -- is "large and expected to grow" as advances in medicine and technology allow people with such conditions to live longer.
A metabolic disorder underlies the brain effects found in those with Huntington's disease, researchers report in an advance article publishing online October 19, 2006. The article will appear in the November 2006 issue of the journal Cell Metabolism, published by Cell Press.
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