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Mutant SOD1 protein forms intracellular aggregations that inhibit protein degradation. Once these mutant RNA-binding proteins are misfolded and aggregated, they may be able to misfold normal protein both within and between cells in a prion-like manner.
C9orf72 is the most commonly mutated gene in ALS and causes motor neuron death through a number of mechanisms.
The three mechanisms of disease associated with these C9orf72 repeats are deposition of RNA transcripts in the nucleus, translation of the RNA into toxic dipeptide repeat proteins in the cytoplasm, and decreased levels of the normal C9orf72 protein.
Excitotoxicity , or nerve cell death caused by high levels of intracellular calcium due to excessive stimulation by the excitatory neurotransmitter glutamate , is a mechanism thought to be common to all forms of ALS.
Motor neurons are more sensitive to excitotoxicity than other types of neurons because they have a lower calcium-buffering capacity and a type of glutamate receptor the AMPA receptor that is more permeable to calcium.
In ALS, there are decreased levels of excitatory amino acid transporter 2 EAAT2 , which is the main transporter that removes glutamate from the synapse; this leads to increased synaptic glutamate levels and excitotoxicity.
Riluzole, a drug that modestly prolongs survival in ALS, inhibits glutamate release from pre-synaptic neurons; however, it is unclear if this mechanism is responsible for its therapeutic effect.
No test can provide a definite diagnosis of ALS, although the presence of upper and lower motor neuron signs in a single limb is strongly suggestive.
Their sensitivity is particularly poor in the early stages of ALS. Because symptoms of ALS can be similar to those of a wide variety of other, more treatable diseases or disorders, appropriate tests must be conducted to exclude the possibility of other conditions.
While a magnetic resonance imaging MRI is often normal in people with early stage ALS, it can reveal evidence of other problems that may be causing the symptoms, such as a spinal cord tumor, multiple sclerosis , a herniated disk in the neck, syringomyelia , or cervical spondylosis.
Based on the person's symptoms and findings from the examination and from these tests, the physician may order tests on blood and urine samples to eliminate the possibility of other diseases, as well as routine laboratory tests.
ALS must be differentiated from the "ALS mimic syndromes", which are unrelated disorders that may have a similar presentation and clinical features to ALS or its variants.
Myasthenic syndrome , also known as Lambert—Eaton syndrome, can mimic ALS, and its initial presentation can be similar to that of myasthenia gravis MG , a treatable autoimmune disease sometimes mistaken for ALS.
MG is eminently treatable; ALS is not. There is no cure for ALS. Management focuses on treating symptoms and providing supportive care, with the goal of improving quality of life and prolonging survival.
One study found that NIV is ineffective for people with poor bulbar function  while another suggested that it may provide a modest survival benefit.
Physical therapy can promote functional independence   through aerobic, range of motion, and stretching exercises. There is weak evidence that PEG tubes improve survival.
Palliative care should begin shortly after someone is diagnosed with ALS. Hospice care can improve symptom management at the end of life and increases the likelihood of a peaceful death.
Riluzole has been found to modestly prolong survival by about 2—3 months. Edaravone has been shown to modestly slow the decline in function in a small group of people with early-stage ALS.
Other medications may be used to help reduce fatigue, ease muscle cramps, control spasticity, and reduce excess saliva and phlegm.
Depression can be treated with selective serotonin reuptake inhibitors SSRIs or tricyclic antidepressants,  while benzodiazepines can be used for anxiety.
A review concluded that mexiletine was safe and effective for treating cramps in ALS based on a randomized controlled trial from Non-invasive ventilation NIV is the primary treatment for respiratory failure in ALS  and was the first treatment shown to improve both survival and quality of life in people with ALS.
Continuous positive pressure is not recommended for people with ALS because it makes breathing more difficult. As the disease progresses, people with ALS develop shortness of breath when lying down, during physical activity or talking, and eventually at rest.
Respiratory failure is the most common cause of death in ALS. It is important to monitor the respiratory function of people with ALS every three months, because beginning NIV soon after the start of respiratory symptoms is associated with increased survival.
This involves asking the person with ALS if they have any respiratory symptoms and measuring their respiratory function.
Non-invasive ventilation prolongs survival longer than riluzole. A randomized controlled trial found that NIV prolongs survival by about 48 days and improves quality of life; however, it also found that some people with ALS benefit more from this intervention than others.
For those with normal or only moderately impaired bulbar function, NIV prolongs survival by about seven months and significantly improves quality of life.
For those with poor bulbar function, NIV neither prolongs survival nor improves quality of life, though it does improve some sleep-related symptoms.
Invasive ventilation bypasses the nose and mouth the upper airways by making a cut in the trachea tracheostomy and inserting a tube connected to a ventilator.
The person with ALS will continue to lose motor function, making communication increasingly difficult and sometimes leading to locked-in syndrome , in which they are completely paralyzed except for their eye muscles.
However, invasive ventilation imposes a heavy burden on caregivers and may decrease their quality of life.
Physical therapy plays a large role in rehabilitation for individuals with ALS. Specifically, physical, occupational, and speech therapists can set goals and promote benefits for individuals with ALS by delaying loss of strength, maintaining endurance, limiting pain, improving speech and swallowing, preventing complications, and promoting functional independence.
Occupational therapy and special equipment such as assistive technology can also enhance people's independence and safety throughout the course of ALS.
Range of motion and stretching exercises can help prevent painful spasticity and shortening contracture of muscles. Physical and occupational therapists can recommend exercises that provide these benefits without overworking muscles, because muscle exhaustion can lead to worsening of symptoms associated with ALS, rather than providing help to people with ALS.
Occupational therapists can provide or recommend equipment and adaptations to enable ALS people to retain as much safety and independence in activities of daily living as possible.
People with ALS who have difficulty speaking may benefit from working with a speech-language pathologist. Preventing weight loss and malnutrition in people with ALS improves both survival and quality of life.
People with ALS should eat soft, moist foods, which tend to be easier to swallow than dry, crumbly, or chewy foods. Palliative care , which relieves symptoms and improves quality of life without treating the underlying disease, should begin shortly after someone is diagnosed with ALS.
If people with ALS or their family members are reluctant to discuss end-of-life issues, it may be useful to use the introduction of gastrostomy or noninvasive ventilation as an opportunity to bring up the subject.
Hospice care , or palliative care at the end of life, is especially important in ALS because it helps to optimize the management of symptoms and increases the likelihood of a peaceful death.
ALS is the most common motor neuron disease in adults and the third most common neurodegenerative disease  after Alzheimer's disease and Parkinson's disease.
Men have a higher risk mainly because spinal-onset ALS is more common in men than women. The incidence in these areas has decreased since the s;  the cause remains unknown.
People of all races and ethnic backgrounds may be affected by ALS,  but it is more common in whites than in Africans, Asians, or Hispanics.
The Midwest had the highest prevalence of the four US Census regions with 5. The Midwest and Northeast likely had a higher prevalence of ALS because they have a higher proportion of whites than the South and West.
ALS can affect people at any age,  but the peak incidence is between 50—75 years  and decreases dramatically after 80 years.
One thought is that people who survive into their 80s may not be genetically susceptible to developing ALS; alternatively, ALS in the elderly might go undiagnosed because of comorbidities other diseases they have , difficulty seeing a neurologist, or dying quickly from an aggressive form of ALS.
This will largely be due to the aging of the world's population, especially in developing countries. Flail leg syndrome, another regional variant of ALS, was first described by Pierre Marie and his student Patrikios in In , American naval doctors reported that ALS was times more prevalent among the Chamorro people of Guam than in the rest of the world.
It was then approved in Europe in and in Japan in In Edward H. Therefore, amyotrophia means "no muscle nourishment,"  which describes the loss of signals motor neurons usually send to muscle cells;  this leads to the characteristic muscle atrophy seen in people with ALS.
Lateral identifies the areas in a person's spinal cord where the affected motor neurons that control muscle are located. Sclerosis means "scarring" or "hardening" and refers to the death of the motor neurons in the spinal cord.
ALS is sometimes referred to as "Charcot's disease" because Jean-Martin Charcot was the first to connect the clinical symptoms with the pathology seen at autopsy.
The term is ambiguous and can also refer to Charcot—Marie—Tooth disease and Charcot joint disease. In the United States and continental Europe, the terms "ALS" or "Lou Gehrig's disease" refer to all forms of the disease, including classical ALS, progressive bulbar palsy, progressive muscular atrophy, and primary lateral sclerosis.
The contestants then dump the buckets of ice and water onto themselves. However, it can be done in a different order. Many different organisms are used as models for studying ALS, including Saccharomyces cerevisiae a species of yeast ,  Caenorhabditis elegans a roundworm , Drosophila melanogaster the common fruit fly , Danio rerio the zebrafish , Mus musculus the house mouse , and Rattus norvegicus the common rat.
It expresses about 20—24 copies of the mutant human SOD1 gene  and reproduces most of the clinical and pathological findings seen in ALS.
Both of these methods are faster and cheaper than traditional methods of genetically engineering mice; they also allow scientists to study the effects of a mutation in mice of different genetic backgrounds, which better represents the genetic diversity seen in humans.
Cellular models used to study ALS include the yeast Saccharomyces cerevisiae and rat or mouse motor neurons in culture.
Small-animal models include the fruit fly, the roundworm C. Of the three, the fruit fly is the most widely used; it has a rapid life-cycle, short lifespan, a sophisticated nervous system, and many genetic tools available.
From the s until , about 50 drugs for ALS were tested in randomized controlled trials RCTs ; [h] of these, riluzole was the only one that showed a slight benefit in improving survival.
Drugs tested and not shown to be effective in clinical trials in humans include antiviral drugs, anti-excitotoxic drugs, growth factors, neurotrophic factors, anti-inflammatory drugs, antioxidants, anti-apoptotic drugs, and drugs to improve mitochondria function.
An analysis of 23 large phase II and phase III RCTs that failed between and concluded that there were many potential reasons for their lack of success.
These trials in humans went ahead on the basis of positive results in SOD1 transgenic mice, which are not a good animal model for sporadic ALS.
Additionally, in most preclinical studies the SOD1 mice were given the drug during the presymptomatic stage; this makes the results less likely to apply to people with ALS, who begin treatment well after their symptoms begin.
Positive results in small phase II studies in humans could also be misleading and lead to failure in phase III trials. Other potential issues included the drug not reaching its intended site of action in the central nervous system and drug interactions between the study drug and riluzole.
Repetitive transcranial magnetic stimulation had been studied in ALS in small and poorly designed clinical trials; as of [update] , evidence was insufficient to know whether rTMS is safe or effective for ALS.
As of [update] it appeared that differences in the methylation of arginine residues in FUS protein may be relevant, and methylation status may be a way to distinguish some forms of FTD from ALS.
Amyotrophic lateral sclerosis. For other uses, see ALS disambiguation. Main article: Genetics of amyotrophic lateral sclerosis.
See also: List of people with amyotrophic lateral sclerosis. Play media. Main article: Amyotrophic lateral sclerosis research. The judge in the case concurred, and in the NFL agreed to pay an unlimited amount of damages for players found to have ALS, Parkinson's disease , Alzheimer's disease , or dementia.
Orphanet Journal of Rare Diseases. National Institute of Neurological Disorders and Stroke. Archived from the original on 13 April Retrieved 7 November Archived from the original on 5 January Retrieved 2 January Nature Reviews.
The Cochrane Database of Systematic Reviews. Food and Drug Administration. Archived from the original on 8 May Journal of Neurology, Neurosurgery, and Psychiatry.
NHS Choices. Archived from the original on 29 December Disease Primers. The Lancet. Bibcode : PLoSO Revue Neurologique.
Morbidity and Mortality Weekly Report. Archives of Neurology. Encyclopedia of human genetics and disease. Santa Barbara, CA: Greenwood. Archived from the original on 8 September Jacoby, Robert M.
Encyclopedia of family health 3rd ed. Tarrytown, NY: Marshall Cavendish. Nature Neuroscience. Brain Research. World Health Organization.
Retrieved 24 January Neurologic Clinics. Cold Spring Harbor Perspectives in Medicine. Neural Plasticity. Amyotrophic Lateral Sclerosis.
Journal of Neurologic Physical Therapy. Journal of the Neurological Sciences. The New England Journal of Medicine. Archived from the original on 19 September Retrieved 18 September Journal of Neurology.
Amyotrophic Lateral Sclerosis Journal Article. Lay summary — Massachusetts General Hospital 11 May Archived from the original on 15 August The Neuroscientist.
Annals of Translational Medicine. Diseases of the Nervous System. Academic Press. Retrieved 2 May Trends in Genetics. Epidemiologic Reviews.
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