A team of researchers at the University of California discovered a new compound identified as AF267B to be effective in reducing the 2 types of brain lesions common in Alzheimer’s disease - beta amyloid plaques and tangles.
According to Dr. Frank LaFerla, professor of neurobiology and behavior and co-director of the UCI Institute for Brain Aging and Dementia, AF267B mimicks a chemical in the brain, the acetylcholine, which is essential for learning and memory. People suffering from Alzheimer’s diesase suffer a significant loss of neurons that produce the acetylcholine. Compounds that mimicked acetylcholine, also known as M1 agonists, have so far failed the clinical trials.
Alzheimer’s transgenic mice, which were injected with AF267B daily for 8 weeks were better able to remember the location of a hidden platform compared to those which were injected with a placebo. When the brains of the transgenic mice were examined there were fewer plaques and tangles for those treated with AF267B than for those receiving only a placebo. AF267B had no effect on normal mice which were not afflicted with plaques and tangles. However both normal and transgenice mice were unable to locate the platform when injected with dicyclomine, a M1 antagonist (a M1 antagonist performs the opposite function of a M1 agonist) and they all showed an increased amount of plaques and tangles.
LaFerla’s research team also showed that the buildup of beta-amyloid plaques triggers the development of Alzheimer’s disease and removal of them from the brain cleared up the tangles. This is known as the Amyloid Cascade hypothesis.
Although Dr. Laferla realized that the effects of AF267B on human beings are still unknown he believes it is a tremendous step forward in the treatment of Alzheimer’s disease.
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