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 the quest to understand the driving forces behind neurodegenerative diseases, researchers in recent years have zeroed in on clumps of malfunctioning proteins thought to kill neurons in the brain and spinal cord by jamming their cellular machinery.
Scientists from Harvard Medical School have identified a key instigator of nerve cell damage in people with amyotrophic lateral sclerosis, or ALS, a progressive and incurable neurodegenerative disorder.
Amyotrophic lateral sclerosis (ALS, or Lou Gehrig's disease) is a progressive disorder that devastates motor nerve cells. People diagnosed with ALS slowly lose the ability to control muscle movement, and are ultimately unable to speak, eat, move, or breathe.
MIT engineers have developed a microfluidic device that replicates the neuromuscular junction -- the vital connection where nerve meets muscle.
Harvard Stem Cell Institute researchers at Harvard University and the Broad Institute of Harvard and MIT have found evidence that bone marrow transplantation may one day be beneficial to a subset of patients suffering from amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disorder more commonly known as Lou Gehrig's disease.
USC researcher Megan L. McCain and colleagues have devised a way to develop bigger, stronger muscle fibers. But instead of popping up on the bicep of a bodybuilder, these muscles grow on a tiny scaffold or "chip" molded from a type of water-logged gel made from gelatin.
A phase II clinical trial in people with amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease, suggests that transplanting human stem cells into the spinal cord may be done safely.
A study led by biomedical researchers at Indiana University has found evidence that an enzyme known as NMNAT2 may help protect against the debilitating effects of certain degenerative brain diseases, including Alzheimer's.
Follicular helper T cells (Tfh cells), a rare type of T cells, are indispensable for the maturation of antibody-producing B cells. They promote the proliferation of B cells that produce highly selective antibodies against invading pathogens while weeding out those that generate potentially harmful ones.
University of Florida Health researchers have developed a unique mouse model that will allow researchers around the world to better study the genetic origins and potential treatments for a neurodegenerative brain disease that causes amyotrophic lateral sclerosis, often referred to as ALS or Lou Gehrig's disease, and frontotemporal dementia.
Cedars-Sinai research scientists have found that immune cells in the brain play a direct role in the development of amyotrophic lateral sclerosis, or ALS, offering hope for new therapies to target the neurodegenerative disease that gradually leads to paralysis and death.
Scientists at Rutgers and Stanford universities have created a new technology that could someday help treat Parkinson's disease and other devastating brain-related conditions that affect millions of people.
The Independent Citizens Oversight Committee of the California Institute for Regenerative Medicine approved yesterday a $6.3 million grant to a research team from the University of California, San Diego School of Medicine and University of California, Davis to pursue a novel human embryonic stem cell-based therapy to rescue and restore neurons devastated by amyotrophic lateral sclerosis or ALS.
Malfunctioning mitochondria — the power plants in cells — are behind the damage caused by strokes, heart attacks, and neurodegenerative diseases, but little has been known about how to stop these reactors from melting down, destroying cells and tissue. Mitochondria also take up calcium, which regulates energy production.
A new study led by scientists at The Scripps Research Institute suggests that cells construct protein "clumps" to protect against neurodegenerative diseases such as amyotrophic lateral sclerosis, a.k.a. ALS or Lou Gehrig's disease.
A small peptide dubbed TAxI is living up to its name. Recent studies show it to be an effective vehicle for shuttling functional proteins, such as active enzymes, into the spinal cord after a muscle injection.
Researchers at Oregon State University announced today that they have essentially stopped the progression of amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease, for nearly two years in one type of mouse model used to study the disease - allowing the mice to approach their normal lifespan.
J. Gavin Daigle, a PhD candidate at the LSU Health New Orleans School of Graduate Studies, is the first author of a paper whose findings reveal another piece of the Amyotrophic Lateral Sclerosis (ALS) puzzle.
An analysis funded by the National Eye Institute (NEI), part of the National Institutes of Health, has identified three genes that contribute to the most common type of glaucoma. The study increases the total number of such genes to 15.
St. Jude Children's Research Hospital scientists have developed a web application and data set that gives researchers worldwide a powerful interactive tool to advance understanding of the mutations that lead to and fuel pediatric cancer. The freely available tool, called ProteinPaint, is described in today's issue of the scientific journal Nature Genetics.
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