{"cache":{"posts_f30bc_67337":{"__typename":"RootQueryToPostConnection","nodes":[{"__typename":"Post","id":"cG9zdDoyMjAxNg==","databaseId":22016,"featuredImage":null,"author":null,"date":"2014-12-15T06:00:25","uri":"/articles/study-says-genetics-may-play-larger-role-in-als","title_b28e9_bf21a":"Study Says Genetics May Play Larger Role in ALS","slug":"study-says-genetics-may-play-larger-role-in-als","categories_3cd3e_bf21a":{"__typename":"PostToCategoryConnection","edges":[{"__typename":"PostToCategoryConnectionEdge","node":{"__typename":"Category","id":"dGVybToxNTQx","slug":"health-traits","name":"Health + Traits","uri":"/category/health-traits","seo":{"__typename":"TaxonomySEO","title":"News Archives - 23andMe Blog","opengraphTitle":"News Archives","metaDesc":"23andMe News are blog post where our research or innovative products have pushed new boundaries that are worth sharing and make news.","opengraphDescription":"23andMe News are blog post where our research or innovative products have pushed new boundaries that are worth sharing and make news.","fullHead":"\n\n\n\n\n\n\n\n\n\n\n\n\n"}}}]},"imageOptions":{"__typename":"Post_Imageoptions","featuredImageSquare":{"__typename":"MediaItem","id":"cG9zdDo0NjQ1","mediaDetails":{"__typename":"MediaDetails","sizes_cad4b_bf21a":[{"__typename":"MediaSize","name":"thumbnail","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2009/09/Gehrig1-150x150.jpg"},{"__typename":"MediaSize","name":"medium","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2009/09/Gehrig1-222x300.jpg"},{"__typename":"MediaSize","name":"square_sm","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2009/09/Gehrig1-271x271.jpg"},{"__typename":"MediaSize","name":"square_md","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2009/09/Gehrig1-372x372.jpg"},{"__typename":"MediaSize","name":"square_lg","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2009/09/Gehrig1-443x574.jpg"},{"__typename":"MediaSize","name":"wide_sm","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2009/09/Gehrig1-271x149.jpg"},{"__typename":"MediaSize","name":"wide_md","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2009/09/Gehrig1-372x204.jpg"},{"__typename":"MediaSize","name":"wide_lg","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2009/09/Gehrig1-443x315.jpg"},{"__typename":"MediaSize","name":"wide_xl","sourceUrl":"https://blog-api.23andme.com/wp-content/uploads/2009/09/Gehrig1-443x539.jpg"}],"height":600,"width":443},"mediaItemUrl":"https://blog-api.23andme.com/wp-content/uploads/2009/09/Gehrig1.jpg","sourceUrl_772ce_bf21a":"https://blog-api.23andme.com/wp-content/uploads/2009/09/Gehrig1.jpg"},"singleTemplateFeaturedImage":null},"content_b28e9_bf21a":"

A new study suggests that genetics plays a much bigger role in ALS than previously thought.
\n $\"Lou$
\nPast estimates said genetics accounts for about 10 percent of cases. But a new study by researchers at Cedars-Sinai and Washington University in St. Louis suggest that as many as one in three cases of ALS can be tied to genetics.

The finding sheds light on the possible genetic origin of the disease. This is important particularly for patients who have had no family history for it.

Lou Gehrig’s Disease

Amyotrophic Lateral Sclerosis, also known as Lou Gehrig’s Disease, is a rare neurodegenerative disease. It is marked by a wasting of nerve cells that control the muscles in your body. It is often fatal. Right now there is no cure for ALS. In 90 percent of the case, clinicians cannot point to a cause. It was thought that most of those so-called “sporadic” cases were the result of environmental factors.

But this new study in the Annals of Neurology, suggests that genetics may play a role in many of those cases.

The Genetics

Previous studies have identified about a dozen genetic variants associated with ALS. Among those are variants in the C90RF72 gene and in another gene, SOD1. But the Cedar-Sinai and Washington University study identified many more rarer variants associated with ALS. Researchers suggest that alone these variants may not have a big impact, but acting in combination they do.

The hunt for the causes and possible treatments for ALS got a boost over the summer through the viral spread of the “ALS Ice Bucket Challenge” social media campaign.

The campaign generated some pretty good videos. More importantly for researchers the campaign brought in close to $100 million during the summer. The ALS Association, recently gave researchers at Cedar-Sinai $1.6 million to support their work on the disease.

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$\"Lou$

Amyotrophic Lateral Sclerosis (ALS) is a rare and deadly neurological disorder affecting voluntary muscle movement. It typically claims victims’ lives about three years after symptoms begin. In the United States, the condition is more commonly known as Lou Gehrig’s disease, after the Yankees slugger who died of ALS in 1941. About 20,000 people in the U.S. have ALS and one in 100,000 people develop the disease per year.

Despite years of research, relatively little is known about the causes and risk factors of ALS. This week, understanding of the disease moved a step forward with a study published in PNAS that identified several new genetic variants associated with ALS risk.

A team of scientists led by Francois Gros-Louis and Jean-Pierre Julien of UniversitÃ© Laval in Canada analyzed genetic variants in the CHGB gene in more than 700 French and Swedish people with ALS and 750 people without the disease. Although most of the variants found in the CHGB gene were rare, one of the more common variants was markedly more frequent in those with ALS than in those without. The rarer T version of this SNP was associated with about 2.4 times increased odds of ALS, compared to the more prevalent C version. The SNP also seemed to affect age-of-onset: individuals with the T version of tended to develop ALS about 10 years earlier than individuals with two copies of the C version.

One of the hallmarks of ALS and some other neurodegenerative diseases is the abnormal aggregation of proteins within cells. Many of these aggregations appear in organelles known as the endoplasmic reticulum (ER) and the Golgi network, which are tasked with processing proteins into their mature forms and readying certain ones to be secreted, or released outside the cell.

Gros-Louis and his team focused on the CHGB gene because of its “guilt-by-association” relationship with SOD1, one of the few established genetic factors linked to ALS. Abnormal SOD1 proteins tend to aggregate in motor neurons of people with ALS, and recent reports have found chromogranin B, the protein encoded by CHGB, near these aggregates.

Chromogranin B is typically secreted from cells like a hormone, and so the researchers hypothesized that genetic variants in CHGB associated with increased risk for ALS might impair secretion of chromogranin B. Sure enough, in cells with CHGB containing the T version of , almost all of the protein remained sequestered inside the ER/Golgi network. In cells with normal CHGB, only 40% of the chromogranin B protein was found there.

Previous studies in this area have indicated that stress and damage to the ER and Golgi are a defining characteristic of ALS-affected motor neurons. Gros-Louis and his colleagues suggest that further research be done to investigate whether CHGB variants like stress the ER-Golgi system and hasten the deterioration of motor neurons.

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Scientists are narrowing in on two regions of the human genome that could be responsible for ALS (amyotrophic lateral sclerosis), also known as Lou Gehrig’s disease.

ALS is a neurodegenerative disorder that weakens muscles and paralyzes patients within three years of onset, and has no known cure. The available drug treatment delays progression by only three to five months.

Despite several attempts to find genetic variations associated with the sporadic form of the disease (which accounts for 95% of ALS cases), no association has been found.

A team of researchers from Netherlands, Van Es et al., analyzed the genes of nearly 20,000 people of European descent, including 5,000 ALS patients. Their results, published online this week in Nature Genetics, identified several genetic variations on two chromosomes suspected to affect ALS and other neurological functions.

The study revealed that each copy of the C version of a SNP on chromosome 19, is associated with a 1.2 times increased odds of ALS compared to having two copies of A. This SNP is found near UNC13A, a gene that may be involved in the function of motor neurons, which degenerate and die in ALS patients.

Another SNP ,located on chromosome 9, is associated with a 1.16 times increased odds of ALS. This SNP was found in a region of the genome previously associated with the rare familial (non-sporadic) version of ALS. Researchers also found an association between the disease and a third SNP located very close to .

There is increasing evidence that ALS belongs to a broader spectrum of neurodegenerative disorders, including Parkinson’s disease, so researchers speculate that genetic associations with ALS may also lead to clues about other disorders of the nervous system.

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ALS

Study Says Genetics May Play Larger Role in ALS

A New Genetic Variant Associated with ALS Risk and Age-of-Onset

Genetic Variations May Increase Risk for ALS

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