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An experimental vaccine stopped cognitive decline in mice with Alzheimer's disease

The goal: reducing precipitation

Alzheimer's disease frustrates neuroscientists. Although the number of people with it is increasing, there is still no way to diagnose it, it is impossible to predict who will get sick and how the disease will develop, and no medicine has been found that will eliminate it or alleviate its symptoms over time. In three articles published today in the journal Nature, researchers report that they succeeded in vaccinating mice with Alzheimer's disease. The vaccine reduced the brain damage and even gave the mice protection against the deterioration in memory and learning ability, which characterize the disease.

Alzheimer's disease is characterized by changes in brain tissue and dementia (dementia). It is difficult to determine which changes in the brain tissue are responsible for the development of dementia. Two theories try to explain this. According to one theory, the causes of dementia are clusters of protein particles called beta-amyloid that form outside the brain cells. But the researchers are not yet clear whether the beta-amyloid clusters are the causes of the disease or are its by-products,
formed after the death of brain cells. If indeed they are the causes of the disease, then if it is possible to prevent their formation, or break them down in some way, it will be possible to directly treat the cause of the disease and prevent its spread. This is the central question in Alzheimer's disease, and the answer to it will only be known if a treatment is found that will eliminate the protein deposits.

According to the second theory, the cause of the development of Alzheimer's disease is a protein called tau, which also accumulates in the brains of patients. If this assumption is correct, treatment to prevent the formation of beta-amyloid will not have the same effect on the symptoms of the disease.

To study Alzheimer's disease in a living system, scientists tried to make an animal develop the disease, with all its symptoms, similar to humans. This became possible after it was discovered that a mutation in the gene that codes for the starting protein of beta-amyloid causes, in a small percentage of Alzheimer's patients, the onset of the disease. If the damaged human gene is inserted into fertilized mouse eggs, the mice that develop from the eggs develop some of the symptoms of human Alzheimer's disease, such as the accumulation of beta-amyloid deposits in the brain, changes in the neurons, a decrease in the number of neurons in the forebrain and changes in behavior.

A year ago, an article was published in "Nature" in which it was reported that a vaccine consisting of beta-amyloid segments was able to considerably lower the formation of beta-amyloid clumps in the brains of mice that expressed the symptoms of human Alzheimer's disease. However, it was not possible to show whether the vaccine can also ward off the cognitive symptoms of the disease, which make coping with it so difficult. In the three articles published today, the researchers addressed this question, and the results of their research raise the hope that the vaccine will reduce the extent of dementia affecting patients.

The researchers imposed various tasks, which require learning and short-term memory (which is the main victim of Alzheimer's), on mice that received the vaccine component and on mice that were not vaccinated, and tested over time how they coped with them.

As happened in the previous experiment, there was a decrease in the amount of beta-amyloid deposits formed in the brains of the vaccinated mice. But more than that, the vaccine gave the animals protection against the cognitive deterioration that characterizes Alzheimer's disease. The mice that were vaccinated with the beta-amyloid particles performed the tasks given to them much better than the sick mice that did not receive the vaccine, and their learning ability and memory were impaired to a lesser extent than the other mice. The beta-amyloid vaccine thus provided protection against the severe dementia symptoms that increase with age, and also reduced the accumulation of beta-amyloid deposits in the brain.

"The studies are an important breakthrough in understanding the pathological process of Alzheimer's disease," says Dr. Zeev Meiner from the neurology department at Hadassah Ein Kerem Hospital, "but it is important to note that the mouse model does not contain all the pathological findings that appear in the brains of humans with Alzheimer's disease. For example, the pathological findings related to the tau protein are not expressed in the brains of the experimental mice, so it is not clear whether a vaccine based on the beta-amyloid protein will prevent the damage that may be caused by the tau protein. A combined vaccine of several proteins may be necessary to cure the disease."
{Appeared in Haaretz newspaper, 21/12/2000{

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