Theoretically the disease could be stopped in its tracks by halting transmission from cell to cell—maybe with a tau-blocking antibody. The study results will have immediate implications for developing new treatments, according to researchers working independently at Columbia and Harvard. They likened imagined treatments for halting the disease to treating cancer while in its early stages before it has spread.
For many years researcher tried to unravel the mystery of how AD spreads. Did lesions pop up independently of one another throughout the brain, or did AD spread outward like contagion from the memory center where it first emerges?
The means to the solution was provided by genetically engineering mice to accumulate abnormal human tau proteins in the entorhinal cortex, where cells first start to die in AD. Following the mice over two years yielded the information they were looking for. Since human tau proteins could not spontaneously appear in isolated pockets of mouse brains, they could only arrive at other areas via transmission from cell to cell.
As researchers mapped the path of the human tau protein they saw it spread outward from the entorhinal cortex to hippocampus to neocortex—the same progression as seen in humans. Researchers are now asking whether other degenerative brain diseases, such as Parkinson’s, may spread the same way.
The Columbia University study was done by Karen Duff and Dr. Scott A. Small and their colleagues at the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain at Columbia University Medical Center and was published in the journal “PLoS One”. Another study was led by Dr. Bradley T. Hyman, Director of the Alzheimer’s Disease Research Center at Massachusetts General Hospital and was published in the journal “Neuron”.