A fascinating experiment has Alzheimer Research heading off in a new direction. Stuart Feinstein, professor of Molecular, Cellular and Developmental Biology, and co-director of UCSB’s Neuroscience Research Institute, and his research team found that when they added amyloid beta to neuronal cells, the tau in those cells did not act as predicted but completely fragmented within one to two hours of exposure. Within 24 hours, the cells were dead.
Tau is a key component in the cell’s cytoskeleton and Feinstein argues that neurons die in Alzheimer’s disease because their cytoskeleton is not working properly. “If you destroy tau, which is an important regulator of the microtubules, one could easily see how that could also cause cell death,” said Feinstein. “We know from cancer drugs that if you treat cells with drugs that disrupt the cytoskeleton, the cells die,” he said. “In my mind, the same thing could be happening here.”
The team is busy working on the implications of this experiment and what it might mean for the development of drugs to take aim at the amyloid beta peptide.