Word: miceli
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Dates: during 2000-2009
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Doing it in monkeys, however, could save lives. For more than a decade, researchers have been working with so-called knock-out and knock-in mice--rodents that have had genes added or effectively subtracted from their genome. By observing these custom-made lab animals, researchers have gleaned invaluable information about the workings of hundreds of illnesses, including arteriosclerosis, sickle-cell anemia and nearly every variety of cancer that afflicts people...
...mice are different from people; they aren't perfect laboratory stand-ins. They don't age precisely the way people do, for example. They don't have monthly menstrual cycles, and their neurological and immune systems differ in important ways. Much better to have a more closely related animal with body systems that are more like ours--which is why primate center senior scientist Gerald Schatten and his colleagues decided to try manipulating the genes of the Rhesus monkey, a close cousin to humans and already the mainstay of many medical experiments...
...says Bristol-Myers' Molinoff. "But there's now intriguing evidence that suggests you can get plaque regression." Some of the most striking evidence comes from studies of a vaccine against beta amyloid that Schenk and his co-workers at Elan have developed. In 1999 they administered their vaccine to mice whose brains were filled with plaques. A short time later, the plaques shrank. Currently the Elan vaccine, like the Bristol-Myers' secretase inhibitor, is in early-phase clinical trials, in which the primary objective is to test for safety as opposed to effectiveness...
...discovery of leptin in 1994 that got the genetic study of obesity rolling, and it was Friedman's research team that was responsible. Studying the genome of a rare strain of hugely obese mice, the investigators found that all of them shared a defect in a gene that coded for a previously unknown hormone released by body fat. When a normal animal gains too much weight, the hormone signals the brain to turn down the appetite rheostat. When fat stores drop, the hormone is shut off, causing appetite to rebound. In the gene-damaged mice, there was no leptin...
...announcement of leptin's discovery was big news to biologists, particularly after Friedman administered it to the obese mice and saw their weight drop by a dramatic 30% within as little as two weeks. A next, obvious step was to look for humans with the same defective gene. In Britain, endocrinologist Stephen O'Rahilly of the University of Cambridge did find a pair of leptin-deficient children, one of whom at age 9 weighed a staggering 208 lbs. After modest leptin treatments were begun, both children began dropping weight at a steady rate that sometimes exceeded 4 lbs. a month...