Experimental Drug Reverses Alzheimer's-Type Brain Lesions
For the first time, an experimental drug has been successful in reducing two types of brain lesions present en Alzheimer's disease. The tests were done on mice which had been genetically modified to show the symptoms and the brain lesions common to Alzheimer's. The tests demonstrated that the compound AF267B slowed and reversed the formations of both beta-amyloidal plaques and the presence of fiber tangles of the tau protein in the brains of the mice. These types of brain lesions are common in people with Alzheimer's disease. It is believed that the growth of these types of protein masses is caused by, or is the result of, the death of brain neurons. It is further believed that the presence of these lesions is the physiological explanation of loss of brain function and memory.
In addition to its success in reducing cerebral lesions, the experimental drug also demonstrably improved the memory of the mice receiving it.
The investigators, led by Frank LeFerla of the Department of Neurobiology and Behavior at the University of Irvine, in California, U.S.A., used the mice with Alzheimer's to test the experimental drug AF267B. This drug was designed by Abraham Fisher, a scientist at the Israel Institute for Biological Research. Its purpose was to seek to imitate the effects of the neurotransmitter acetylcholine, an essential brain chemical for learning and memory.
Neurotransmitters are the messengers between the cerebral cells. One neuron secretes a chemical (the neurotransmitter) that then adheres to a receptor of another neuron creating an effect on it. In Alzheimer's disease there is a great loss of neurons that produce acetylcholine and of receptors to receive it. This experimental drug was intended to imitate the work of acetylcholine and of its receptor, M1. The strategy apparently worked. After eight weeks of receiving the drug, the mice with Alzheimer's were successful in completing tasks that demanded the use of their memories.
The drug must next be tested with human subjects. The first clinical studies are being developed by TorryPines Therapeutics, a company located in La Jolla, California.
The article describing the tests, which appeared in the March 2, 2006 issue of NEURON magazine, concludes with, "In conclusion, AF267B represents a peripherally administered low molecular weight compound to attenuate the major hallmarks of AD and to reverse deficits in cognition. Therefore, selective M1 agonists may be efficacious for the treatment of AD."
Things that work with laboratory mice do not always work with humans, but they often do. Beta-amyloidal plaques and tau protein tangles are prominently associated with Alzheimer's patients. This is the first time something has been found to not only slow their formation but actually reverse the formation process! This is very encouraging.]
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