In a study with genetically modified mice, a team of UCI researchers led by Frank LaFerla, professor of neurobiology and behavior, found that a compound known as AF267B, developed by paper co-author Abraham Fisher of the Israel Institute for Biological Research, reduced both plaque lesions and tangles in brain regions associated with learning and memory. Although drugs exist on the market today to treat the symptoms of Alzheimer's, AF267B represents the first disease-modifying compound, meaning it appears to affect the underlying cause and reduces the two signature lesions, plaques and tangles.
The researchers report their findings in the March 2 issue of Neuron.
"AF267B could be a tremendous step forward in the treatment of Alzheimer's disease," said LaFerla, who serves as co-director of the UCI Institute for Brain Aging and Dementia. "Not only does it appear to work on the pathology of Alzheimer's and ease its symptoms, it crosses the blood-brain barrier, which means it does not have to be directly administered to the brain, a significant advantage for a pharmaceutical product. Although we cannot determine what the effects of AF267B will be in humans until clinical trials are complete, we are very excited by the results our study has yielded."
According to LaFerla, AF267B works by mimicking the effects of the neurotransmitter acetylcholine, a chemical in the brain essential for learning and memory. Neurotransmitters act as carriers for messages between brain cells and bind to receptors on the cells' surfaces. Acetylcholine generally binds to specific receptors in the brain, including the M1 receptor, a potentially novel therapeutic target for Alzheimer's disease.
Contact: Farnaz Khadem
University of California - Irvine