Word: onset
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Dates: during 2000-2009
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Almost overnight, it seemed, scientific interest in the genetics of beta amyloid exploded. Researchers had long been aware that early-onset Alzheimer's, while rare, often ran in families. Could it be, they wondered, that the culprit was a mutant version of the APP gene? In 1991 scientists at London's St. Mary's Hospital Medical School screened the DNA of an Alzheimer's family and found what every geneticist in the field had been furiously looking for. The mutant APP gene sat on chromosome 21, and the single change in its DNA sequence occurred in the vicinity...
Sometime later, two more early-onset Alzheimer's genes were found, Presenilin-1 and Presenilin-2. Like APP, these genes were dominant; a child who received just one gene from either parent would inevitably get the disease. One of the most tragic examples involved a 4,000-member Colombian family that had been haunted for generations by Alzheimer's. Yet such cases, researchers were only too well aware, accounted for merely a small fraction of all cases of Alzheimer's disease. Still other genes, they reasoned, must be involved in the great majority of cases--those in which dementia does...
...Allen Roses, a rapier-tongued contrarian then at Duke University, challenged the beta-amyloid orthodoxy. He announced that he and his colleagues had found a major Alzheimer's-susceptibility gene that affected the late-onset forms of the disease. It was the gene for APOE4, a common variant of the APOE lipoprotein, which is one of the many workhorses of the body's cholesterol-transport system. What, everyone wondered, could this lipoprotein, a known risk factor for heart disease, possibly have to do with Alzheimer's? Very quickly, many concluded that Roses could not be right...
...APOE4 may contribute to the development of more than 60% of all late-onset Alzheimer's cases. But that leaves the other 40% unaccounted for. And at this moment, many scientists, including Roses, are racing to identify still other Alzheimer's-susceptibility genes. Rudolph Tanzi, a geneticist from Harvard, believes that he has nabbed a prime suspect on chromosome 12, a gene called A2M. But he has yet to convince his critics. Two years ago, when Tanzi presented his data at an Alzheimer's meeting in Amsterdam, his evidence was brutally attacked. "I wish I'd been wearing chain mail...
...APOE4 and other as yet undiscovered susceptibility genes will produce clues that point to other potential compounds. For as he notes, Alzheimer's disease, no less than heart disease and diabetes, will almost certainly be found to have multiple causes. For example, the genes implicated so far in early-onset Alzheimer's all lead to an overproduction of beta amyloid. But the genes involved in the bulk of cases, Selkoe strongly suspects, are more likely to do with faulty clearance mechanisms that aren't doing a good enough job flushing out the plaques. A sink can overflow, he observes...