Researchers say the studies that analyzed the genes of more than 50,000 people in the United States and Europe, can process to reveal little doubt that the five genes more likely to make the disease in the elderly and have something important about the disease. You can also lead to ways to make your onset delay or slow down the progress.
"The level is the evidence very, very strong,", said Dr. Michael Boehnke, Professor of Biostatistics at the University of Michigan and external consultants in the research. The two studies published Monday in the journal Nature Genetics.
For years it was unproven, but persistent evidence, that include cholesterol and inflammation of the disease process. People with high cholesterol levels are more likely to get the disease. Also encephalitis cause strokes and head injuries, which make more likely, Alzheimer's disease. This line of thinking, some of the newly discovered genes now strengthen because some involved with cholesterol and others are with inflammation or the transport of molecules within the cells.
The discoveries to participate in twice as many genes to Alzheimer's, up to 10 of 5, the scientists, many new fields of consideration known. One who said the papers 155 authors, Dr. Richard Mayeux, Chairman of Neurology at Columbia University Medical Center, the results "field would open up."
And an expert who was figuring out not part who said studies, Dr. Nelson B. Freimer, which Director of Center for neuro-psychological Genetics at the University of California, Los Angeles, now thought there were enough unique genes for Alzheimer's disease, which could make real progress researchers their biology. "This is a large, solid step," he said.
An estimated 5.4 million Americans have Alzheimer's disease, of which most older. According to the Alzheimer's Association have one in eight people older than 65 the disease. The annual cost of the nation is 183 billion $.
By itself, the genes are not nearly as important a factor as APOE, a gene discovered this 1995 greatly increased risk for the disease: 400 percent if a person a copy of a parent, by 1,000 percent if from both parents inherits.
On the other hand the new genes, each increases risk by not more than 10 to 15 percent; for this reason are not to decide them, whether a person is likely to develop Alzheimer's are used. APOE that is involved in emergent cholesterol, "in a class of its own," said Dr. Rudolph Tanzi, Neurology Professor at the Harvard Medical School and author of one of the papers.
But the researchers say that even a slight increase in the risk will help them in understanding the disease and the development of new treatments. And like APOE, seem some of newly discovered genes with cholesterol be included.
Of 10 genes now known, at the age of Alzheimer's disease be assigned to four in the last few years found were and are confirmed by the new studies. APOE may have different roles in the disease, disable the brain of amyloid, which towers participated in plaques, the barnacle like particles that dot a pathological feature of the disease are the brain of Alzheimer's patients and perhaps.
It is known that one of the first signs of Alzheimer's disease is a collection of beta-amyloid or a beta, a protein that forms plaques. And it is known, later in the disease, distorted and confused displayed proteins - Tau - in the dead and dying nerve cells.
But what is not known why the a-beta starts to get, why the brains of people with Alzheimer's that get rid of excess cannot be, or what is the connection between amyloid and Tau.
One of the new fonts by the American researchers analyzed the genes of 54,000 people, some with Alzheimer's and other in the same age but without the disease. They found four new genes.
The other paper's researchers in the UK, France and other European countries with contributions from the United States. It confirms the genes of the American researchers found and another gen added.
The American study started three years ago when Gerard D. Schellenberg, pathology professor at the University of Pennsylvania, the national institutes of health with a complaint and a proposal went. Individual research groups had their own studies but not much success done genome, because no one had enough topics center.
Dr. Schellenberg said in an interview that he Dr. Richard j. Hodes, told Director of the National Institute on Aging, had to stop the small genomic studies, and Dr. Hodes had agreed.
These days, Dr. Hodes said "The old model, in which researchers jealously guarded their data, is no longer applicable."
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