In two similar articles published in Time Magazine and The New York Times, the movement of the tau protein is traced as it spreads across the brain of mice. Tau is thought to be responsible for actively killing cells in AD, by piling up inside and overwhelming them. Another implicated protein in the disease is beta amyloid, which is secreted and piles up around the cells. The amyloid is thought to 'set the stage' for the tau proteins, creating an unfavorable environment for the brain. While there is no reason to believe that the amyloid moves amongst neurons, researchers at Columbia and Harvard independently seem to have obtained evidence that the tau protein travels in the brain analogous to how a bacterium is spread throughout the body. In their research, specific parts of the brain were genetically altered to produce the tau protein - normally found in humans and not mice - in the entorhinal cortex, where it originates in AD. The tau proteins proceeded to kill the cells of the entorhinal cortex; however, surrounding areas also died and evidence was found for the spread of the protein to these additional areas. Since the mice were only modified to produce the tau in an isolated area, evidence of it in other places is only possible through the physical transmission of the protein across neurons. This explanation is consistent with our knowledge of AD progression and one of two prevalent theories for the progression of AD, which describes it as a spreading virus of sorts.
There is also growing evidence for a similar explanation of the progression of Parkinson's Disease, the second most common form of neurodegeneration. The growing knowledge of the physical progression of these diseases may have grand implications for their treatment. If the tau proteins are the direct cause of AD progression, then the isolation of tau infected areas may allow the symptoms to be likewise contained and the progression of the disease to be slowed, if not halted. This finding and the research that will surely follow it may provide enough evidence to inspire the production of drugs that target the implicated proteins and to ultimately alter the current passive method of care for AD patients, possibly even offering a 'cure'.
The New York Times
by Gina Kolata
by Alice Park
Posted by James Fargnoli (1)