Two studies, one done at Columbia and the other at Harvard, reported the unexpected news that Alzheimer's disease appears to spread in the brain when the protein known as tau becomes defective and infects one area after another. The process seems to be similar to the way viruses or bacteria spread infectious diseases.
The researchers believe that the discovery signals the potential for developing treatments not only for Alzheimer's but also for other degenerative brain diseases such as Parkinson's. Scientists have been aware for years that dying tau cells initially show up in the area of the brain where memories are stored and then move outward, claiming other mental functions of Alzheimer's patients. However until now, researchers have not been able to pinpoint exactly how the disease progresses. These new studies provide an explanation at last and they offer the tantalizing hope that the inexorable decline that is typical of Alzheimer's could be stopped in its tracks, possibly with an antibody.
Both studies were done in mice but the researchers expect that the process is the same in humans because the mice had a human tau gene. The study led by Karen Duff and Dr. Scott A. Small was done at the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at Columbia University Medical Center and was published on February 1st in the peer-reviewed online journal PLoS One. The second study was led by the director of the Alzheimer's Disease Research Center at Massachusetts General Hospital and is slated to be published in the journal Neuron.
