New research suggests that your skills behind the wheel may be affected by your genes.

To better understand the effects of a variant in the BDNF gene on motor skills learning, Steven Cramer and colleagues at UC Irvine tested 29 subjects in a driving simulator. Their results, published in the journal Cerebral Cortex, might make you think twice about whom you go on your next road trip with.

Subjects sat in front of a screen with their hands firmly planted at “10 and 2″ on a steering wheel and guided their “car” around a track, attempting to stay centered over a black line. The steering was tuned so that subjects had to begin turning before the screen actually changed.

Over the course of 15 trials, all of the study subjects got better at the driving task. But the seven people who had a T rs6265 improved less than those with two Cs. When subjects returned to the lab four days later for a final lap, everyone had forgotten how to drive the simulator a little bit, but those with a T did worse.

“These people [with a T at rs6265] make more errors from the get-go, and they forget more of what they learned after time away,” Cramer said in a press release.

(23andMe customers can check their data for rs6265 using the Browse Raw Data feature.)

The BDNF protein helps to regulate how nerve cells make new connections and maintain old ones. The T version of rs6265, also known as the Val66Met variant, reduces the amount of BDNF available in the brain and has been linked to impaired learning and memory. Studies have shown that stroke victims with this variant don’t recover as well as those who lack it.

But there may be an upside: the variant seems to have a beneficial effect on cognition in people with Parkinson’s disease, Huntington’s disease, lupus and multiple sclerosis.

“It’s as if nature is trying to determine the best approach,” Cramer said. “If you want to learn a new skill or have had a stroke and need to regenerate brain cells, there’s evidence that having the variant is not good. But if you’ve got a disease that affects cognitive function, there’s evidence it can act in your favor. The variant brings a different balance between flexibility and stability.”

See Wired Science for more.

SNPwatch gives you the latest news about research linking various traits and conditions to individual genetic variations. These studies are exciting because they offer a glimpse into how genetics may affect our bodies and health; but in most cases, more work is needed before this research can provide information of value to individuals. For that reason it is important to remember that like all information we provide, the studies we describe in SNPwatch are for research and educational purposes only. SNPwatch is not intended to be a substitute for professional medical advice; you should always seek the advice of your physician or other appropriate healthcare professional with any questions you may have regarding diagnosis, cure, treatment or prevention of any disease or other medical condition.

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A new report in the Journal of the American Medical Association adds to the mounting evidence that genetic variations impact the efficacy of clopidogrel (Plavix®), a drug used to prevent blood clots in people who have had a heart attack or stroke and also those with peripheral artery disease and unstable angina.

Previous research has shown that certain variations in the CYP2C19 gene prevent the body from converting clopidogrel into its active form. That reduces the amount of anti-clotting effect people get from the medication, increasing their risk for heart attacks, strokes and death from cardiovascular causes.

(23ndMe customers can learn how their data fits in with this research in a previous Spittoon post or in the Clopidogrel Efficacy Drug Response Report.)

The researchers, led by Alan Shuldiner of the University of Maryland School of Medicine, determined that BMI, lipid levels and age account for about 10% of the variation in clopidogrel’s ability to prevent blood clotting. Variation in the CYP2C19 gene accounted for another 12%, meaning that other factors, probably both genetic and non-genetic, are also at work.

For patients whose genetics may reduce the benefits of clopidogrel treatment, there are other options. Prasugrel (Effient®) was recently approved by the FDA and appears not to be affected by the same variations that impact clopidogrel efficacy, although there are some concerns about bleeding caused by this drug.  Several other drugs (ticagrelor, cangrelor, elinogrel) that could be used for clotting reduction in place of clopidogrel are currently in clinical trials.

Clinical trials have not yet been conducted to show if identifying people with variants of the CYP2C19 before prescribing clopidogrel actually improves health outcomes.  If such studies do show a benefit and this type of testing becomes routine, people with these variants might be steered away from clopidogrel by their doctors, which would seem to be a boon for the makers of newer medications.

But in an editorial accompanying the study in JAMA, Deepak Bhatt suggests that testing for these variations would also allow physicians to know for whom clopidogrel will work (probably). This would be an important piece of information considering that the patent on clopidogrel is set to expire in 2011, so cheaper generic forms of the drug will be available then.

“Although such testing currently is expensive, the cost will decrease and hopefully will coincide with supportive data.  Furthermore, if such testing allowed use of a less expensive generic anitplatelet drug, the test might essentially pay for itself,” he writes.

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Researchers have identified a genetic variant that increases risk of atrial fibrillation (AF), an electrical disorder of the heart, which in turn increases risk of stroke.

AF affects one in four people over 40 years old, and stroke is the third leading cause of death in the United States.

In one of two studies, scientists scanned the genomes of 5,806 people from the United States, Iceland and Norway to look for genetic variations associated with AF. The other study combined data from several large studies comprising almost 47,000 people of European ancestry.

Their results, published online this month in Nature Genetics, newly linked one SNP to slightly elevated risk for developing AF in European populations.

Most strokes are caused by a blood clot that blocks circulation to the brain. Because AF causes ineffective beating of the heart, blood can pool and clot in the upper chambers, resulting in stroke if a clot leaves the heart and lodges in the brain. AF increases the risk of stroke four to five times across all age groups and is the cause behind 10 to 15 percent of all blood clot-related strokes.

In the first study, Gudbjartsson et al. studied people of European descent from the United States, Iceland and Norway to reveal that the T version of rs7193343, a SNP on chromosome 16, is associated with 1.21 times increased odds of AF. This SNP was also associated with 1.11 times increased odds of ischemic stroke and 1.22 increased odds for cardioembolic stroke.

In the second study, Benjamin et al. associated AF with another SNP near rs7193343. Both SNPs are likely to be marking a third genetic variation that actually has a functional effect on AF. Further research will be necessary to identify both the variation and its effect.

(23andMe customers can check their data for rs7193343 using the Browse Raw Data feature.)

Gudbjartsson et al. also assessed the association of AF with the T version of rs7193343 in more than 3,000 Han Chinese, but the association was not significant. They noted that the T allele of this SNP is much more frequent in Han Chinese than in European populations.

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It has been known for decades that having the gum disease periodontitis increases a person’s risk for heart attack (free registration required), stroke and other forms of cardiovascular disease. Research suggests that the link is due to inflammation in the gums causing an immune reaction throughout the entire body. That can increase blood pressure and encourage the accumulation of atherosclerotic plaques in the arteries.

Now researchers have drawn a genetic link between periodontitis and heart disease as well. It turns out that variations in a region of chromosome 9 that have already been associated with heart disease also influence a person’s chances of developing periodontitis.

The specific genetic marker identified by the study is not part of the 23andMe Personal Genome Service. But another marker that has also been linked to heart disease and lies in the same chromosomal neighborhood is described in the Heart Attack research report.

Arne Schäfer of the Institute for Clinical Molecular Biology in Kiel, Germany presented the research in Vienna, Austria, last week at the annual meeting of the European Society of Human Genetics. He and his colleagues found that people with a marker for increased cardiovascular risk in a stretch of DNA known as 9p21 were more likely to have gum disease as well.

The high-risk version of the marker increased a person’s chances of having generalized aggressive periodontitis by 1.99 times, and localized aggressive periodontitis 1.72 times. Aggressive periodontitis generally strikes early in life and progresses rapidly, leading to tooth loss as early as age 20.

The 9p21 region of chromosome 9 contains several genes involved in suppressing the proliferation of cells. In a recent PLoS Genetics paper the researchers suggest that the variation they studied somehow affects the function of one of these genes.

Rather than superceding previous findings linking the effects of periodontal inflammation itself on heart disease, the researchers said, their study provides valuable additional information that could help unravel the connection between the two conditions.

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Researchers have identified a genetic variation that may raise the risk for stroke by affecting brain cells’ ability to respond to injury.

Stroke is the third leading cause of death in the United States, striking almost 800,000 people each year. High blood pressure, high cholesterol, smoking, diabetes, obesity and a history of cardiovascular disease can all increase the risk of having a stroke, but studies of families and twins indicate that genes play a substantial role too.  So far, however, the genes underlying stroke risk in the general population remain undetermined.

Scientists combined data from several large studies comprising almost 29,000 people from the United States and the Netherlands to look for genetic variations associated with stroke risk. Their results, published online today in the New England Journal of Medicine, link a region of the genome not previously associated with stroke to increased risk in both black and white populations.

Strokes can be either hemorrhagic (caused by a broken blood vessel that bleeds into or around the brain) or ischemic (caused by a blood clot that blocks blood flow to the brain). Most strokes are the ischemic type.

Combined analysis of data from Caucasian study participants from the United States and the Netherlands revealed that the A version of rs12425791 is associated with a 1.29 times increased risk of ischemic stroke.  The SNP was also associated with an increased risk for ischemic stroke in a large African American study group – 1.42 times for each copy of an A.  Analysis of a smaller group of African Americans failed to yield a significant association between rs12425791 and stroke.

(23andMe customers can check their data for rs12425791 using the Browse Raw Data feature.)

The risk of stroke is almost doubled for African Americans compared to white Americans, and African Americans are more likely to die from stroke or complications from stroke than any other ethnic group.

Rs12425791 is located near the NINJ2 gene, which encodes a protein that has been implicated in nerve cell injury response in animal studies.  Several other SNPs in and around the NINJ2 gene showed modest association with stroke. The authors of the study suggest that SNPs affecting how much protein is made from the NINJ2 gene might influence the brain’s response when deprived of oxygen by a blood clot.

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For the millions of Americans who suffer from migraines, the risk of throbbing pain that can last for days is plenty to worry about.  But studies have shown that having a propensity for these severe and sometimes disabling headaches can also increase the risk for cardiovascular events such as stroke and heart attack.

In new report published this week in Neurology, researchers using data from the Women’s Health Study suggest that only those women with a specific genetic variation and whose migraines include aura, a type of visual disturbance characterized by flashing lights and patterns, are at increased risk for cardiovascular disease (CVD).

Previous studies have attempted to link both migraines and CVD with a variation referred to as the D/I polymorphism in ACE, a gene that encodes a blood vessel-constricting protein.  Drugs that inhibit the ACE protein are used to treat migraines and CVD.

In a study that included 25,000 women with European ancestry, about 3,200 of whom had migraines, Schürks et al. found no association of the D/I polymorphism with the headaches. Over 12 years of follow-up, there were 625 cardiovascular events (mainly strokes and heart attacks) in the group, but again, no association with the D/I polymorphism.

When the researchers took genetics out of the equation, they found that a woman with a history of any type of migraine was about 30% more likely to have CVD.  But when they added genetics back in and also divided the migraneurs (people who get migraines) up based on the presence or absence of aura, they found that only those women who had migraine with aura and also had the DD or DI genotype at the ACE polymorphism were at about two-fold increased risk for CVD.

(23andMe customers can check their data using SNP rs1799752 in the Browse Raw Data feature.  Data for this SNP is available only to those customers who received their data after 9/1/08, or upgraded their accounts since that date.)

Although these results may eventually help scientists understand the exactly how migraine and CVD are related to ACE, a lot of work remains to be done.  The authors themselves warn that larger studies will be needed and that their research did not take into account environmental or other genetic risk factors.  They also note that their study sample was restricted to Caucasian women 45 years old and older, which may mean that their results are not applicable to the population as a whole.  Finally, in both women with and without migraine, the proportion of the different genotypes (DD/DI/II) differed from what would be expected in the population, suggesting that there may have been flaws in the study.

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