While the findings offer no immediate new perspective on the disease or treatments, they offer more support for the growing belief that a single protein, beta amyloid, is responsible for Alzheimer's disease.
Groups with Mayo Clinic in Jacksonville, Fla., Boston's Harvard Medical School and Washington University School of Medicine, St. Louis, publish their research in Friday's issue of the journal Science.
Researchers do acknowledge that in the absence of any current vaccine or effective treatment, information about genetic risk factors stirs as much anxiety as curiosity on the part of the general public.
"The studies add to the relatively long list of genetic regions linked to an increased risk of developing Alzheimer's disease. These factors will take on importance when we have preventive therapy. Until then, they confirm the idea that there is not going to be a simple solution with this disease," said Bill Thies, a vice president with the National Alzheimer's Foundation in Chicago.
Alzheimer's Disease is a progressive degenerative condition, characterized by neurofibrillary tangles in the brain and deposits, or plaques, of beta amyloid. These disorders lead to loss of memory and physical function and finally to death.
While the accumulation of beta amyloid has been genetically linked to early-onset Alzheimer's, one of the three studies in Science -- by Dr. Steven Younkin of the Mayo Clinic in Jacksonville Florida and colleagues -- is the first to link plasma levels of the protein to the development of Alzheimer's late in life.
Another group, led by Rudolph Tanzi of Harvard Medical School, focused on a slightly different region of chromosome 10, near a gene for an insulin-degrading enzyme that may be involved in breaking down beta amyloid.
"The three studies strengthen the beta amyloid hypothesis and suggest that there may be a gene in this region of chromosome 10 that affects the very production of the protein, " said Alison Goate of Washington University School of Medicine, St. Louis, and lead investigator on one of the studies.
Goate and her colleagues reviewed the genetics of hundreds of pairs of siblings, each of whom had developed Alzheimer's disease. That analysis also led them to suspect a specific region on chromosome 10 was linked to susceptibility to the disease.
For the past several years, a gene on chromosome 19 has been the single widely-recognized risk factor for late onset Alzheimer's disease. Although investigators around the world have searched intensively for other genes, no clear culprit has emerged.
"One big problem in genetics is that groups frequently cannot replicate one another's findings. The Science papers are noteworthy, because three different groups all implicated the same, relatively small, area of chromosome 10," commented David Morgan, director of the Alzheimer's Research Laboratory at the University of South Florida at Tampa.
The discovery of the region, while a cause for excitement in the Alzheimer's research community, is just the beginning of the more difficult challenge.
"It is just the preamble to finding the culprit gene, an effort which can take years," added David Westaway, a molecular biologist at the University of Toronto who specializes in Alzheimer's studies in animal models.
Both researchers and patient-support organizations are aware that with the discovery of new genetic risk factors for Alzheimer's disease, public concern grows about the potential use and misuse of such information.
"Until recently, most information about genetic risk factors concerned very rare conditions, but that is not the case with Alzheimer's, of course," said Goate. "We are all aware of the theoretical worry that such genetic profiling information could be used to discriminate against someone with risk factors for such a common disease. That is why ethical considerations as much as scientific ones should influence the course of this kind of research."
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