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Experimental Alzheimer’s Drug curbs the disease in mic

Frank LaFerla, a professor of neurobiology at the University of California, Irvine (UCI) and also the senior author in the research said that the experimental drug// AF267B is effective against both forms of brain lesions found in Alzheimer's disease in mice.

This compound (AF267B) curbs both the amyloid protein plaques that collect in Alzheimer's-affected brains, as well as another lesion, the tangles of protein called tau.

In mice that have been genetically designed to mimic Alzheimer's disease AF267B also appears to reverse cognitive declines. Researchers said that the mice appeared to gain renewed powers of memory and learning after treatment. The findings of the study were reported in the journal Neuron.

AF267B is a perfect drug for the Alzheimer's disease. It has the disease-modifying capacity that treats the symptoms and also reverses the cognitive declines. Frank LaFerla said that AF267B is an M1 agonist. It acts by stimulating the muscarinic receptor which is present on the surface of nerve cells.

In the Alzheimer's disease there is a selective loss of neurons which produce the neurotransmitter acetylcholine. He said that by stimulating the M1 receptor one can boost the acetylcholine activity and AF267B does the stimulation. It was developed by the famous Alzheimer's researcher and study co-author Abraham Fisher, of the Israel Institute for Biological Research, in Ness-Ziona, Israel.

But all this was possible only because of the genetically designed mouse. This mouse mimics human Alzheimer's disease more closely than any previous rodent strain. That's because these mice develop both plaques and tangles whereas the previous models failed to develop tangles.

William Thies, vice president of medical and scientific affairs at the Alzheimer's Association said that this research is the stepping stone to find the cure for human Alzheimer's disease. LaFerla said that in these mice models it was found that when the M1 receptors were stimulated there was a reduction in the two major neuropathological lesions plaques and tangles. After this these mice were given AF267B. They began to perform much better in tests that assessed memory and learning, reversing previous Alzheimer's-linked cognitive dysfunction. Later examination of brain tissue confirmed that the drug appears to target neurons in exactly those brain centers affected by the disease.

On the other hand LaFerla said that success in mice is not always a guarantee of success in human patients. Further research has to be done with various combinations of drugs on these mouse models. He also said that an effective drug should clear both the plaques and tangles.


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