Alzheimer's Disease Vaccine?

PBS's 'Secret Life of the Brain' reviews research on the prevention and treatment of Alzheimer's disease.

Alzheimer's Disease is a tragic illness. A degenerative brain disease that affects one in 10 people over 65, it causes sufferers to become confused and lose their cognitive functions, undoing them mentally and physically with a terrifying relentlessness, scrolling their hard-won adult competencies back to helpless inability to care for themselves, causing them to forget the very faces and names of their loved ones and the memories that help make them who they are. The course of the disease may take years, but it ends in death. Though Alzheimer's is a disease and not a natural result of aging, the risk does increase with age - nearly half of everyone over 85 has Alzheimer's disease. Because the population is aging, the number of Alzheimer's patients in the U.S. is expected to rocket from 4 million now to 14 million by the year 2050. According to some estimates, the annual total cost of caring for Alzheimer's patients in the U.S. is already as much as $100 billion; not to mention the huge cost in human suffering for both patients and caregivers. Finding a treatment for or, better still, a way to prevent Alzheimer's would clearly be a tremendous medical, social and humanitarian boon. So far, there is no medical treatment available to cure or halt Alzheimer's, though drugs exist that may temporarily relieve some symptoms. But it is a tremendously exciting time in Alzheimer's research. Hundreds of promising discoveries have been made in the past few years, and at least one group of researchers may be on the brink of a finding a viable treatment, or at least a greatly improved understanding of what causes the disease. Efforts to find a way to prevent or treat Alzheimer's are proceeding along many different avenues. Here are some of the areas considered most promising: When researchers earlier in this century dissected the brains of deceased Alzheimer's patients, they noticed that the brains were full of two kinds of obviously abnormal structures: what are now referred to as plaques and tangles. Plaques are abnormal build-ups, in the spaces between the afflicted brain's nerve cells, of a kind of protein fragment called beta-amyloid. Tangles are abnormal collections, inside neurons, of twisted threads made up of a protein called tau. For a long time, researchers have struggled to understand whether plaques and tangles are causes or results of Alzheimer's disease, and which of the two is the more significant pathology. Much of the current research is taking the tack that plaque formation is the more significant, and a central process in the disease's terrible progression. In an exciting development, the Irish drug company Elan and Wyeth-Ayerst Laboratories in New Jersey, working jointly, announced in July 2001 that they are about to begin human testing of a new Alzheimer's "vaccine" that could halt or even cure the disease. The "vaccine," called AN-1792, contains bits of beta-amyloid. When injected into a person's arm, it will -- its developers hope -- stimulate the body's antibodies to seek out and remove the foreign intruder, beta-amyloid, just as a flu vaccination stimulates the body's antibodies to the flu virus. This immune response, hopefully, will clean out the beta-amyloids forming plaques in the brain. The vaccine has been shown to be somewhat successful in mice and safe in humans. The new human tests, set to begin in the fall of 2001, should show whether it works to treat people with Alzheimer's. "Everybody is excited about AN-1792," said Bill Thies, vice president of medical and scientific affairs for the Alzheimer's Association. "It is going to be the first test of a critical theory about Alzheimer's disease -- whether lowering levels of amyloids halts the progression of the disease. Even if it fails, you'll have a very important piece of information about the disease causes and process." Meanwhile, other teams of researchers are looking for ways to block or prevent the production of amyloids in the brain in the first place. Other researchers are pursuing the implications of some interesting findings from population studies: that people who take high doses of anti-inflammatory drugs, and women who take estrogen, develop Alzheimer's at a lower-than-expected rate. Some researchers now believe that brain inflammation may play a part in the development of Alzheimer's, and are investigating whether anti-inflammatories and estrogen (which has an anti-inflammatory effect on nerve cells) can be used to prevent or delay Alzheimer's. Others are investigating the effect of diet, specifically of restricting calories, since calorie restriction may also prevent brain inflammation and perhaps therefore the development of Alzheimer's. Increasing Supplies of a Chemical Messenger One significant cause of Alzheimer's symptoms is the fact that, as the disease progresses, it destroys the brain's ability to produce an important chemical messenger called acetylcholine. The medications that are already in use to treat Alzheimer's symptoms, mentioned above, all work by blocking an enzyme that breaks down acetylcholine, thus preserving more for the brain to use. Some researchers are now focusing on tackling the shortage from a different angle, by increasing production of acetylcholine. A Cholesterol Connection? Still other researchers are testing the idea, gleaned from some population and animal studies, that cholesterol may play a role in Alzheimer's development. In 2002, there will be a large trial to see if taking cholesterol-lowering statin drugs can slow down the progression of clinical signs of the disease in patients with mild to moderate Alzheimer's. The above are only some of a wealth of different avenues in research to prevent and/or treat Alzheimer's. Bill Thies of the Alzheimer's Association summed up the held-breath quality of this moment in time: "Waiting for the results of all these trials going on right now is like being a mother hen sitting on a bunch of eggs, waiting for the first beak to pop out."

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  • Source: DNALC.G2C

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