It's too soon to celebrate, however. Other vaccines proved successful in mice, but were unexpectedly dangerous for humans.
In 1999, scientists at Elan and Wyeth-Ayerst Laboratories developed a vaccine that was successful in mice. Early trials in humans were promising, but research was halted in 2002 when the vaccine caused caused severe brain inflammation in 6% of patients. That seems like a small number, but it is far too large for safety.
The current vaccine hopes to avoid this side effect by using a DNA sequence that codes for amyloid beta (Ab) peptides , which results in a more gentle action in the brain. Muscle cells recognize the DNA at the point of injection, and the Ab peptide is produced. Then antibodies are created by the immune system in the body, and the antibodies cross into the brain. This vaccine has produced no brain swelling or bleeding in mice.
The vaccine has reduced the appearance of amyloid proteins -- the proteins responsible for the 'plaques' found in the brains of Alzheimer's Disease patients -- by significant amounts. The results of the study will be published in the Federation of American Societies for Experimental Biology journal in July 2007. If it can do the same thing for humans, without causing dangerous side effects, we'll have a really important advance in fighting Alzheimer's Disease.
We may not have a cure, however. There's no real way to know whether the beta amyloid plaques are a cause of Alzheimer's Disease, a result of the disease, or a separate characteristic altogether. The plaques can only be reliable located by an autopsy. In living patients, Alzheimer's Disease is clinically diagnosed by a series of observations and medical tests. When clinically diagnosed patients die and their brains are autopsied, the characteristic plaques are not always present. Experts disagree on how closely the results of clinical diagnosis and autopsies agree. Some say that the results are the same in about 90 per cent of cases, while others say that the results are the same only about 40 per cent of the time.
It's possible that a vaccine that successfully halts the development of beta amyloid plaques may not have much effect on the set of symptoms now clinically diagnosed as Alzheimer's Disease. Even that, however, would be a step forward in understanding this terrible disease. We would, at the least, know whether the plaques are responsible for the disease or only an indicator, and that would give us guidance in developing treatment methods.
Published by Lou Paun
I'm a retired teacher, a mother, a homeowner . . . and a joyous writer! View profile
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