Q: In this task, you are given a text of many news articles seperated by special token "|||||". Your task is to summarize them.
Gene May Protect Against Alzheimer’s Disease 
  
 Results Provide Boost for Drugs in the Pipeline Targeting the Gene 
  
  
  
 WebMD Health News By Denise Mann WebMD Health News 
  
 WebMD News Archive 
  
 July 11, 2012 -- Can Alzheimer's disease be prevented? 
  
 A new study shows that researchers might be on the right path to someday make it happen. New research has identified a genetic mutation that may protect against both Alzheimer's disease and age-related declines in thinking and memory. And future drug treatments already in the pipeline may help prevent against both. 
  
 Amyloid protein plaques in the brain are seen in people with Alzheimer's disease. A gene for amyloid-beta precursor protein (APP) plays a key role in the formation of these plaques. Researchers from Reykjavik, Iceland, found that a mutation in this gene may help protect against Alzheimer's disease and age-related mental decline. 
  
 This mutation is rare, but, when present, confers about a 40% reduction in amyloid plaque-forming proteins. What's more, study participants between 80 to 100 years old without Alzheimer's disease who carry this mutation have better mental function than those without the mutation, the study shows. 
  
 The findings appear in Nature. 
  
 Alzheimer's disease affects memory and thinking. Symptoms usually develop slowly and worsen with time. One in eight older Americans has Alzheimer's disease, making it the most common type of dementia in the U.S., according to the Alzheimer's Association. 
  
 New Research Is on Target 
  
 U.S. Alzheimer's disease researchers are enthused about the new findings and what they may mean for prevention. 
  
 "This is an extraordinary paper," Sam Gandy, MD, PhD, says in an email. He is the Mount Sinai chair in Alzheimer's disease research at Mount Sinai School of Medicine in New York City. "This provides some of the strongest evidence ever that amyloid is the right target in Alzheimer's." 
  
 Many researchers are developing treatments that target amyloid protein. "Amyloid researchers the world over couldn't have asked for a better morale booster," he says. "This is a great gift to those at high risk for future development of Alzheimer's disease because this means our prevention trials are aiming at the right target." 
  
 But, "for those already suffering, this will have little benefit in terms of new drugs soon," Gandy says. 
  
 "This article is fascinating, as it supposes that there may be a spectrum of progression in Alzheimer's disease," says Richard Isaacson, MD. He is an associate professor of clinical neurology and the director of the Alzheimer's division at the University of Miami Miller School of Medicine. "We are learning more and more about the influence of genetics on cognitive decline and Alzheimer's disease." ||||| Mutations that cause Alzheimer’s lead to excessive amounts of beta amyloid in the brain; by contrast, the protective mutation slows beta amyloid production, so people make much less. 
  
 “This paper provides strong evidence that it would work in the general population if you did it right,” Dr. Altshuler said. 
  
 Scientists at the drug companies agreed. “We are thrilled,” said Ryan Watts, one of the authors of the new paper and head of the neurodegeneration labs at Genentech, which is developing two drugs to reduce brain amyloid levels. 
  
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 Dr. Richard Mohs, leader of neuroscience early clinical development at Eli Lilly, said the company was “very encouraged by these study results.” They show, he said, that despite an initial failure, the strategy of focusing on drugs to reduce beta amyloid levels is “a logical path for the development of effective therapies that may slow disease progression.” 
  
 Many questions remain, of course. Most people do not have the protective gene mutation, but as common as Alzheimer’s is, most people do not get it. It is not clear why. And most who develop Alzheimer’s do not have one of the rare gene mutations that cause it. The reasons for their disease are unclear. 
  
 The discovery of the protective gene mutation, a product of the revolution that has taken place in genetics, arose when researchers scanned the entire DNA of 1,795 Icelanders. 
  
 About 1 in 100 had a mutation in the gene for a large protein that is sliced to form beta amyloid. Then the investigators studied people who had been given an Alzheimer’s diagnosis, and a group of people 85 and older. Those with the mutation appeared to be protected from Alzheimer’s disease. 
  
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 The investigators, led by Dr. Kari Stefansson, chief executive at DeCode Genetics, an Icelandic company, looked at genomes of North Americans and found the gene mutation in only about 1 in 10,000 people. That indicates, Dr. Stefansson said, that the mutation arose relatively recently in Scandinavia. 
  
 The protective gene even appears to override a very strong risk factor for Alzheimer’s disease in old age — two copies of a gene known as ApoE4. Ninety percent of people with two ApoE4 genes get Alzheimer’s by age 80. But Dr. Stefansson says there are 25 people in his study with two copies of ApoE4. None have Alzheimer’s disease. 
  
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 The research “is obviously right,” said John Hardy, an Alzheimer’s researcher at University College London and a discoverer of the first gene mutation found to cause the disease. “The statistics and the finding are pretty secure.” 
  
 The discovery is part of a continuing story that implicates beta amyloid as a central and crucial player in this destructive brain disease. The idea began two decades ago with the discovery of very rare gene mutations that always cause Alzheimer’s in those who inherit them, usually by middle age. The mutations were different in different families, but all had the same effect: They increased the amount of beta amyloid in the brain. That meant that a buildup of amyloid was sufficient to cause the disease. 
  
 Elderly people with Alzheimer’s — who typically do not have these gene mutations — also had excess amyloid in the brain. So researchers reasoned that might mean that excess amyloid was causing the disease in them, too. 
  
 Photo 
  
 Additional evidence of the role of beta amyloid was reported on Wednesday in The New England Journal of Medicine. Using spinal taps and brain scans to track the protein, investigators found that people with one of the Alzheimer’s-causing mutations start making too much beta amyloid as long as 20 years before they have symptoms of the disease. 
  
 Researchers and drug companies focused on the amyloid hypothesis to the extent that almost every experimental drug being tested to slow or halt Alzheimer’s disease is designed to reduce the amount of amyloid in the brain. Most of those drugs are still being tested in clinical trials, but a Lilly drug that failed spectacularly in 2010, semagacestat, actually made people with Alzheimer’s worse and gave rise to soul-searching in the field. 
  
 It emphasized a crucial question that hung over the endeavor. Was amyloid really causing Alzheimer’s in elderly people? Might the protein instead be a bystander, accumulating, for example, as part of the brain’s response to damage? 
  
 The discovery of the protective gene mutation provides strong clues. People with the mutation make substantially less beta amyloid, but other than that they are no different from anyone else. And they do not get Alzheimer’s. 
  
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 People could be tested to see if they have the protective mutation, Dr. Stefansson said, but he added, “The benefits of doing so are not obvious to me.” He explained that since the gene is so rare, chances that a person being tested would have it — especially if that person is not Scandinavian — are extremely low. Almost everyone would end up with the same uncertainty they have now. There is as yet no way to prevent Alzheimer’s and, outside of families with one of the rare disease-causing gene mutations, no way to know who is going to get it. 
  
 Still, Dr. Hardy noted, as provocative as the discovery of the protective gene mutation is, the strategy of reducing amyloid levels — the ultimate test of the amyloid hypothesis — still must be evaluated in typical Alzheimer’s disease. For example, perhaps people need to have lower levels of beta amyloid from birth to really be protected. 
  
 Researchers and companies explain away the failure of the first few experimental drugs to reduce beta amyloid levels or to block the protein by saying they were not powerful enough and were studied in people who already had the disease and clear symptoms of mental decline. By then it might be too late to make any difference. When brain cells have died, nothing can bring them back. 
  
 The strategy now is to use new brain scans and other methods to find and treat people before they have symptoms of mental decline. 
  
 “The idea is that treatment has to start early to make a difference,” Dr. Watts said. 
  
 Of course, people with the newly discovered mutation have lower levels of beta amyloid for their entire lives. 
  
 “You couldn’t start earlier than that,” Dr. Watts said. |||||
A:
A new study in Nature offers what looks to be a genuine advance in the fight against Alzheimer's, one that raises hopes for a preventative drug in the future. Researchers discovered that a particular gene mutation prevalent in Icelanders slows the production of a substance called beta amyloid in the brain, reports the New York Times. Excessive amounts of the substance have been linked to the disease, and the study found that elderly people with the anti-amyloid mutation are better protected, notes WebMD. Drug companies have been working on amyloid remedies for a while, so far without success, but the discovery brings strong evidence that they're on the right track—especially if they can mimic the effects of the newly discovered mutation. The finding is "extraordinarily important," says an Alzheimer's expert at the Mount Sinai School of Medicine, calling it the biggest breakthrough in more than 20 years. But "for those already suffering, this will have little benefit in terms of new drugs soon," he adds.