Alzheimer's Vaccine
...f judgement, and loss of abstract thought. Parkinson’s disease can occur during this stage. Hallucinations and delusions are also symptoms seen during the second stage or later. (Rainey, 53) In the third stage of the disease there is a large interruption of all intellectual function with the former personality becoming submerged. During this stage, people might not recognize family, friends, or themselves. Patients become bedridden and lose control over their bodily functions. Patients reach a vegetative state where they can survive for several years. Progressive wasting is followed by death usually caused by pneumonia. (Rainey, 53) Until the cause of AD is determined, a cure remains elusive. Two risk factors have been identified for the cause of AD: advanced age and genetic predisposition. Recent preliminary research has found a hereditary gene called an “apolipoprotein”, that is a necessary part of the human body that helps to metabolize cholesterol, as a risk factor in developing AD. There are no treatments that reverse or retard the progression of the illness. However, scientists recently hypothesized that deposits of a protein called beta-amloyd plaque in the brain could be one of the main reasons for memory loss and dementia suffered by patients afflicted by AD. This new research was published by the South San Francisco, California Elan Pharmaceuticals in July 8, 2000 issue of the journal Nature. In Nature, the pharmaceutical described a new compound called AN-1792 that could prevent the formation of the amloyd plaques. (Hotinski, 3-4) The new findings came about when Elan injected mice with beta-amloyd. The plaque’s main ingredient was beta amloyd, a fragment of a normal body protein that somehow goes crazy in Alzheimer’s. Some patients produce too much beta-amloyd and others do not clear it out of the brain properly. Autopsies almost always reveals buildups of protein fragments, which cause plaque. However, researchers don’t know if the plaques cause Alzheimer’s symptoms or are just a side effect. The immunization they found generated antibodies that prevented the accumulation of beta-amloyd within the mouse brain and also cleared existing amloyd deposits, also known as plaques. “Of course, mice aren’t humans,” said Dale Schenk, Elan’s lead scientist, “but we are still very excited by the possibility of a vaccine.” (Johnagon, 2000). Researchers conducted their experiments on nine 6-week-old mice genetically engineered to develop Alzheimer’s-like plaques. First they gave monthly injections of AN-1792 to young mice that had not yet developed plaque deposits. At 13 months the treated mice had almost no plaques, compared with groups given either no treatment or injections of other compounds. All groups, except those vaccinated with AN-1792, had substantial plaque development. In the second test, year-old mice with existing plaque deposits were injected with AN-1792. Plaque development in treated mice was substantially slowed, relative to untreated mice, and some showed a reduction in plaques. Elan pharmaceuticals theorized that a vaccine made from beta-amloyd would stimulate the immune system to recognize, attack the protein, and produce antibodies against the plaque. “We saw that it completely stopped the further progression of the disease,” Dale Shneck, lead scientist at Elan. “It looks like it might have actually diminished the plaques.” (Morris, 2000) Even with this new discovery, there is still the lingering question of whether the vaccine will work on humans. Elan pharmaceuticals and Dr. Shneck has already tested two dozen American patients with a single dose of the vaccine and suffered no negative effects. Extensive clinical trials in the effectiveness of the vaccine will not begin until 2001 when they can get government permission to start testing on large groups of humans. Shneck and his colleagues then plan to begin testing the immunization approach on people with mild to moderate Alzheimer’s disease. (Squires, AO1) Despite the vaccine’s promise, there are a number of reasons the method that worked on mice may not prevent or halt Alzheimer’s in humans. The first reason is because the amyloid plaques may be a symptom of the disease, rather than the cause. The second reason is because Alzheimer’s patients have other changes in the brain that the mice do not fully exhibit, such as tangles of protein inside nerve cells. The third reason is while detectable genetic flaws are linked to some Alzheimer’s cases, most patients have no telltale markers. As Dr. Zaven Khachaturian, senior medical adviser to the Alzheimer’s Association said, “If we are going to have the maximal effect of this, we need to find out who has the disease, who is at risk, much earlier.” Even with those negative factors, there is still much hope that the vaccine will prove to be effective in humans. (Squires, AO1) In addition to the studies done by Elan Pharmaceuticals, there has been many other groups testing and contributing to find a vaccine for AD. One group interested on finding a cure was Richard Morris of Edinburgh University and Dave Morgan of the University of South Florida College of Medicine, who reported the first evidence that the genetically engineered mice suffered progressive memory loss as the amloyd plaques built up in their brains. The next group was Christopher Janus and his animal science class at the University of Toronto who used a similar compound to AN-1792 and found it effective on mice. The last group was Dennis Selkoe and colleagues at Harvard Medical School who tested a nasal spray version in the same type of genetically engineered mice. Selkoe said at a July 30, 2000 Alzheimer’s meeting that “the lining of the nose contains a spe...