DIRECTIONS: Choose the best answer for each question. Is Agi…
DIRECTIONS: Choose the best answer for each question. Is Aging All In Our Genes? In 1995, Valter Longo, a cell biologist at the University of Southern California who studies aging, began to change the genes of simple organisms like single-celled yeast, creating mutations that allowed them to live longer. The reasons for this varied. Some mutated cells could repair their DNA more effectively than normal cells; others became better able to stop the type of DNA damage that would promote cancer in humans. Others were studying the same processes. In 1996, Andrzej Bartke, a scientist at Southern Illinois University, began messing around with mouse genes that are involved with growth. He showed – not surprisingly – that owing to the fact that the growth hormone1 pathway had been shut down, the mice were smaller. What was surprising was that they had longer lifespans – about 40 percent longer – than normal mice. Could similar processes be at work in humans? Could genetic mutations protect against diseases of age? It was a gray day in the Bronx, and 81-year-old Jean Sisinni paced on a gray carpet in a third-floor room on Morris Park Avenue. As she walked, Sisinni struggled to repeat every other letter of the alphabet (“B, D, F, H”), while the sensor on her forehead measured activity in her brain, and the carpet simultaneously registered the location, path, and speed of every step. “You’re doing great!” said Roee Holtzer, a scientist at Albert Einstein College of Medicine who has been conducting studies of brain function and mobility in the elderly. If this sounds like a scientific variation on the old joke about being able to walk and chew gum at the same time, go ahead and laugh. In a series of studies over the past several years Holtzer and Joe Verghese have shown that the amount of thinking people are able do while they walk and talk predicts the risk of dementia, loss of mobility, and falls. These experiments add to research at Einstein led by Nir Barzilai, an Israeli doctor who in 1998 began a study of three New York centenarians. The Einstein project has since grown to include more than 500 centenarians in and around New York City – all from central Europe and all Ashkenazi Jews, a historically isolated population. In this homogeneous group, research has again revealed a set of genes related to longevity. As they gathered more and more data, the Einstein researchers noticed that the Ashkenazi centenarians had exceptionally high levels of HDL, often called the good form of cholesterol,2 and that the children of these centenarians had even higher levels. This sent them off to analyze the DNA of about a hundred genes known to be involved in breaking down and using of cholesterol. What they found was a variant of a gene known as CETP that was more common in centenarians than in others. When they investigated the centenarian version of the CETP gene, they confirmed earlier research showing that due to this particular gene variant, people were protected against heart disease. They have gone on to show that since people have this gene, they perform better on mental tasks like the “walking while talking” experiments. Einstein’s large and ambitious longevity program is part of a sea change sweeping human genetics research, where the emphasis for the past 20 years has been on the search for so-called disease genes – genes that are linked to certain chronic health problems. Many researchers are now focused largely on the search for protective genes, which seem to keep people from getting disease or from aging. The race to find the keys to longevity has even led scientists to a place that looks increasingly important in setting every individual’s rate of aging: the womb.3 Researchers at Einstein now suspect that our pattern of aging may be set very early, perhaps before we’re born. To study this hypothesis, Francine Einstein and John Greally have been examining subtle chemical markings on the DNA recovered from the blood of babies born in the Bronx and comparing differences in babies who were small, normal, or large. They have found that the pattern of DNA markings in both small and large babies is significantly different from that of normal-size babies. As Barzilai explains it, because of things that influence us before we are even born, our rate of aging may be affected. The fetus,4 in other words, may be father of the old man. 1 A hormone is a chemical from body organs that stimulates cells.2 Cholesterol is a fat-like substance produced by the human body and carried in our blood. 3 The womb is the part of a woman’s body where a baby grows.4 A fetus is a baby before it is born.Why do some people perform better on mental tasks like the “walking while talking” experiments?