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.
A discovery made several years ago in a lab researching asthma at Wake Forest School of Medicine may now have implications for the treatment of amyotrophic lateral sclerosis (ALS), a disease with no known cure and only two FDA-approved drugs to treat its progression and severity.
Two Northwestern University scientists have received a $3.1 million grant from the National Institute on Aging to collaborate and investigate drug therapies for amyotrophic lateral sclerosis.
A novel neck brace, which supports the neck during its natural motion, was designed by Columbia engineers.
Prion proteins are known to cause scrapie – a neurodegenerative condition. It is capable of debilitating damage to the nervous system. Researchers have successfully devised a treatment for this condition which prolonged the lives of the lab mice infected with the prions.
Researchers at the Weizmann Institute of Science have shown in mice that intestinal microbes, collectively termed the gut microbiome, may affect the course of amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease.
What if the missing ‘environmental’ factor in some of our deadliest neurological diseases were really written in our genome?
A compound with potential as a treatment for ALS has gained further promise in a new study that showed it improved the condition of mice whose motor neurons had been damaged by an environmental toxin known to cause features of ALS.
Most of the well-studied proteins in our bodies are like metal; some can change shape easily, like aluminum foil, and others are rigid, like steel beams, but they typically have a solid, well-defined structure.
Amyotrophic lateral sclerosis is a neurological condition that affects motor neurons -- the nerve cells that control breathing and muscles.
Increasing the levels of the anti-aging protein hormone Klotho improves the neurological deficits and prolongs life span in an experimental model with Amyotrophic Lateral Sclerosis.
People who have a high body mass index or who gain weight as they get older may have a lower risk of amyotrophic lateral sclerosis, also known as Lou Gehrig's disease, according to a large study published in the June 26, 2019, online issue of Neurology, the medical journal of the American Academy of Neurology.
There are 15 new cases of amyotrophic lateral sclerosis, or ALS, diagnosed in the U.S. each day. The disease causes patients to slowly lose the ability to speak, eat, move and breathe, and comes with an average life expectancy of two to five years after diagnosis.
Johns Hopkins scientists report that adult cells reprogrammed to become primitive stem cells, called induced pluripotent stem cells, make tiny "cargo packets" able to deliver potentially restorative or repairing proteins, antibodies or other therapies to aged cells.
A special focus on rogue proteins may hold future promise in stopping the progression of nerve cell destruction in people who have amyotrophic lateral sclerosis or frontotemporal dementia.
St. Jude Children's Research Hospital scientists have found that the enzymes ULK1 and ULK2 play a key role in breaking down cell structures called stress granules, whose persistence leads to toxic buildup of proteins that kill muscle and brain cells.
St. Jude Children's Research Hospital scientists have cracked the mystery surrounding the most common genetic cause of amyotrophic lateral sclerosis, or Lou Gehrig's disease.
A University of Texas at Arlington College of Nursing and Health Innovation professor will use a series of grants totaling approximately $6.575 million during the next five years to attack a variety of debilitating musculoskeletal diseases.
While exact causes of amyotrophic lateral sclerosis (ALS) remain unknown, new research shows pesticides and other environmental pollutants advance the progression of the neurodegenerative disease.
A growing collection of anecdotal stories raises the possibility that nerve injury in an arm or a leg can act as a trigger for the development amyotrophic lateral sclerosis, or ALS -- a progressive neurodegenerative disease also known as Lou Gehrig's disease, named after the famous New York Yankee who died of it in 1941.
Ben-Gurion University of the Negev has developed a new artificial intelligence (AI) platform for monitoring and predicting progression of neurodegenerative diseases to help identify markers for personalized patient care and improve drug development.