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.
Working with yeast and human cells, researchers at Johns Hopkins say they have discovered an unexpected route for cells to eliminate protein clumps that may sometimes be the molecular equivalent of throwing too much or the wrong trash into the garbage disposal.
In cells, DNA is first converted to RNA, and RNA is next converted to proteins--a complicated process involving several other steps. Nonsense-mediated RNA decay is a processing pathway in cells that, like a broom, cleans up erroneous RNA to prevent its productive conversion into an aberrant protein, which could lead to disease.
A computer interface that can decipher the thoughts of people who are unable to communicate could revolutionize the lives of those living with completely locked-in syndrome, according to a new paper publishing January 31st, 2017 in PLOS Biology.
A bacterial by-product known to be important in maintaining gut health may slow the progression of amyotrophic lateral sclerosis, or ALS - a progressive, neurodegenerative disease.
Under ordinary circumstances, the protein tau contributes to the normal, healthy functioning of brain neurons. In some people, though, it collects into toxic tangles that damage brain cells.
Illumina, Inc. and Bio-Rad Laboratories, Inc. today announced the launch of the Illumina® Bio-Rad® Single-Cell Sequencing Solution at the J.P. Morgan Healthcare Conference. The comprehensive solution is the first next-generation sequencing (NGS) workflow for single-cell analysis, providing researchers the ability to investigate the coordinated contribution of individual cells in tissue function, disease progression, and therapeutic response.
The Orphan Disease Center in the Perelman School of Medicine at the University of Pennsylvania has established a new Program of Excellence for Motor Neuron Disease.
A tool that uses light to manipulate matter inside living cells has begun to explain how proteins assemble into different liquid and gel-like solid states, a key to understanding many critical cellular operations.
When you're suddenly able to understand someone despite their thick accent, or finally make out the lyrics of a song, your brain appears to be re-tuning to recognize speech that was previously incomprehensible.
Researchers at the Virginia Tech Carilion Research Institute have identified a naturally occurring molecule that has the potential for preserving sites of communication between nerves and muscles in amyotrophic lateral sclerosis (ALS) and over the course of aging -- as well as a molecule that interferes with this helpful process.
Molecular clocks in cells throughout the body control many physiologic changes in a 24-hour day/night circadian rhythm -- among them the timing of sleep and wakefulness.
Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is a progressive, fatal neurological disease that attacks the nerve cells controlling voluntary muscles. No effective treatments have been found.
New research suggests that physical fitness, body mass index (BMI), IQ, and stress resilience in young adulthood may have effects on the risk of developing amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease.
New research at Columbia University's Mailman School of Public Health reveals that foods like fruits and vegetables that are high in antioxidant nutrients and carotenoids are associated with better function in amyotrophic lateral sclerosis (ALS) patients around the time of diagnosis.
Cedars-Sinai regenerative medicine investigators have received approval from the U.S. Food and Drug Administration to test a combination stem cell-gene therapy they developed to stall the progression of amyotrophic lateral sclerosis, a neurological disease that causes progressive paralysis and ultimately death.
Researchers at St. Jude Children's Research Hospital have discovered the way toxic proteins linked to the most common forms of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) incapacitate membrane-less organelles inside cells.
Although only 10 percent of amyotrophic lateral sclerosis (ALS) cases are hereditary, a significant number of them are caused by mutations that affect proteins that bind RNA, a type of genetic material.
Researchers from Ben-Gurion University of the Negev have published a new study that describes a novel molecular mechanism that could lead to the development of new therapies for Amyotrophic Lateral Sclerosis (ALS).
A recently-recognized pathologic protein in the brain may play a larger role in the development of clinical Alzheimer's disease dementia than previously recognized, according to a study by researchers at Rush University Medical Center.
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.
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