Researchers Model Brain Protein to Better Understand Concussions

By Lina Sorg

All concussions have the potential to cause permanent, irreversible brain damage. The prevalence and danger of concussions continues to dominate both official and informal conversation nationwide. Concussion, a movie starring Will Smith about traumatic brain injuries in the NFL that opened in December 2015, sparked further discussion.

Researchers at the University of Pennsylvania are refining a prior mathematical model to better understand concussions at a molecular level. The jarring impact that results in a concussion causes the brain to twist or bounce around in the skull. This rough movement produces chemical changes in the brain and stretches and injures brain cells.

Vivek Shenoy, a materials science and engineering professor, Ph.D student Hossein Ahmadzadeh, and Douglas Smith, a professor of neurosurgery and director of the Penn Center for Brain Injury and Repair, previously modeled a brain protein known as tau, which stabilizes and links microtubules. Tau is also implicated in several neurodegenerative diseases, including Alzheimer’s. Microtubules run down axons, which are the long, slender parts of brain cells that allow for communication between cells. The researchers studied axons in an effort to understand why they break as a result of traumatic brain injuries, despite being elastic and stretchy. Tau’s viscoelastic quality, which is key, is akin to that of Silly Putty that expands when stressed slowly, but breaks upon high impact. The rate and intensity of the applied strain on the brain determines how much tau can stretch before breaking.

Now that same research team is redefining their model to better understand tau’s role in concussions. The new model is more realistic and factors in the presence of two tau proteins in each link between microtubules, rather than just one. It also accounts for the dynamic nature of tau proteins, which detach and reattach to each other every few seconds.

This constant shift permits the microtubules to move without harm, which in turn allows the axons to stretch to twice their normal length. A sudden and aggressive blow (caused by a car crash or football tackle, for example), prevents this movement from taking place, because the tau proteins have no time to untangle and break apart. The force is applied to the microtubules themselves, which breaks the axons and causes the brain damage associated with concussions.

Because this new model closely links tau’s presence with damage to axons, the study might shed light on chronic traumatic encephalopathy (CTE), which results from a buildup of tau in the brain and is often seen in athletes who have experienced multiple concussions. Better understanding of the relationship between axon damage and tau aggregation may ultimately improve preventative measures and treatments for concussions.

Read more about the study, including commentary from the researchers, here.

 Lina Sorg is the associate editor of SIAM News

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