Half of people who live to 85 will develop Alzheimer’s disease — a disturbing statistic. But research into a family in South America has revealed a gene mutation that appears to afford protection, and may lead to a way to treat or possibly even prevent the disease.
Clinical trials for drugs to stop or slow the progression of dementia have not been successful. A recent study attempted to determine how much influence, if any, genetic and lifestyle factors may have on the development of dementia.
The availability of relatively affordable personal DNA genealogy testing has led to an increase in people exploring their family histories. If you are considering this type of testing, you should spend some time preparing yourself for what you may learn, and what you may want to do with that knowledge.
A newly available test offers to provide information about your telomeres, parts of your DNA that are considered markers of aging, but on its own this information is of little value, and you can make beneficial lifestyle changes without paying for a test.
Genetic testing may help identify when certain people may be at risk of having an adverse reaction to medication. Researchers hope that such testing will eventually be lead to the ability to recommend the most effective medication that has the fewest side effects for a specific person’s condition.
The use of pharmacogenomics, the study of how a person’s genes affect the body’s metabolizing of medications, can help doctors predict if a person will have a negative reaction to a particular medication, or whether one drug may provide better results than another. However, this information is just one piece of the puzzle when trying to help find the medication that will provide the greatest benefit with the fewest side effects.
Although the two conditions seem unrelated, Alzheimer’s and heart disease actually share a genetic link. People who have a certain gene variant have both a somewhat elevated heart disease risk and a significantly elevated Alzheimer’s risk. Fortunately, a recent study has suggested that when people know they have this variant, they’re more likely to make healthy lifestyle choices that benefit their heart — and what’s good for the heart is good for the brain.
One of the most dreaded side effects of cholesterol-lowering statins is myopathy, or severe muscle pains. A new test on the market can evaluate whether you’re genetically susceptible to myopathy. But true statin-induced myopathy is uncommon, and most muscle pain a person experiences while taking a statin likely isn’t caused by the statin. So, is this test really worth the (significant) price?
Five seemingly different mental health disorders—major depression, bipolar disorder, schizophrenia, autism, and attention-deficit hyperactivity disorder—may be more alike than we think. A ground-breaking new study has identified four regions of the genetic code that carry same variations in people with these disorders. Two of the affected genes help control the movement of calcium in and out of brain cells. That might not sound like much, but this movement provides a key way that brain cells communicate. Subtle differences in calcium flow could cause problems that, depending on other genes or environmental factors, could eventually lead to a full-blown mental illness. But this work offers tantalizing hints that bipolar disorder, major depression, and schizophrenia—and possibly autism and attention-deficit hyperactivity disorder—may not be so distinct after all, but could be different manifestations of the same underlying disorder. This could change the way we view mental illness and open the door to more effective therapies.
The term “personalized medicine” is still something of an abstract idea. In an audacious experiment, Stanford molecular geneticist Michael Snyder gave it a face—his own—and showed what it can do. Snyder and a large team of colleagues first sequenced his DNA, revealing his complete genetic library. Then they analyzed blood samples he gave every few weeks for two years. This was akin to taking a 3-D movie of his inner workings to observe how genes, the molecules that read and decode them (RNA), the proteins they make, and other substances interact during health and illness. The team saw how Snyder’s body responded to a cold at the very beginning of the study. Midway through, they watched as molecular changes wrought by a respiratory infection tipped him into full-blown diabetes.