In response to an article published by the New York Times, the Sports Legacy Institute shared these words (on Twitter): “Mystery solved? Key Alzheimer’s study may have unlocked mystery of how CTE progresses.” What’s being referenced is the release of information discovered by researchers at Harvard and Columbia, who found that Alzheimer’s disease spreads like an infection—not the spreading of virus or bacteria, but the spread of tau protein.
The involvement of tau protein has long been known to be a part of the process in this disease, but in understanding the ways in which such proteins expand over a period of time within the brain offers a variety of potentialities for neuroscience’s future. The study was done with genetically engineered mice that could create abnormal tau protein, and over a two-year period, the neuronal makeup of the mice displayed a path of destruction headed by tau protein through networks of the brain. What was most important to take from this study was the fat that the tau protein functioned through cell-to-cell transmission.
The new studies provide an answer. And they indicate it may be possible to bring Alzheimer’s disease to an abrupt halt early on by preventing cell-to-cell transmission, perhaps with an antibody that blocks tau.
This process has been heavily debated in the scientific community in recent decades, where there was no clear definition to the ways in which Alzheimer’s disease progressed. Scientists did not agree on whether this process was because of cell-to-cell transmission involving tau protein, or it was because the protein found avenues of invasion through the inadvertent assistance of vulnerable neurons. The unanswerable mystery of Alzheimer’s disease now seems to have found its answer, with regards to this particular question and finding. It is now plausible to conceive a method in which the process of this neurodegenerative process could be sidetracked and treated with positive result.
There are still many questions to be asked and many questions to be answered regarding Alzheimer’s disease, but this has been considered a significant breakthrough in all of efforts of research. It may also generate further questions about Parkinson’s disease, and for the greater purpose of this blog’s intentions, and with consideration of the attention given from the Sports Legacy Institute, this finding might lead us towards more of a better understanding of chronic traumatic encephalopathy.
Chronic traumatic encephalopathy is a neurodegenerative disease of the brain that is related to repetitive head trauma over the course of one’s life, and to this point can only be diagnosed postmortem. It is characterized by buildups of tau protein at the microscopic level in regions of the brain, and has been found in numerous accounts of deceased professional athletes. Could this study take us closer to learning much more about chronic traumatic encephalopathy? Time will tell, but for now and for the sake of the medical community, we can only praise them for their efforts and hope that neuroscience continues to build upon an already thriving foundation. With hope and promise, we will see our medical community come closer to changing the lives of many individuals and families afflicted by such neurological diseases and disorders.
JOHN GONOUDE
