USF Professor Studying Relationship Between Causes of Alzheimer’s and CTE, a Disease Found in Athletes with Head Injuries
Researcher says football players’ brain injuries leading to CTE may start with a ‘planted seed,’ then spread.
Martin Muschol with research assistant Mentor Mulaj, PhD and graduate student Chamani Niyangoda. Photo by Aimee Blodgett
TAMPA, Fla. (May 9, 2016) – A University of South Florida professor is joining a growing number of researchers studying chronic traumatic encephalopathy (CTE), a recently discovered brain disease in athletes who have suffered repeated brain trauma from on-field collisions.
Dr. Martin Muschol, an associate professor of physics at USF who studies Alzheimer’s disease, is investigating the possibility that CTE can start when an on-field collision can generate a “seed” that subsequently induces a systemic spreading of protein abnormality in the brain.
While research on CTE is in the early stages, because of its symptoms many researchers are comparing CTE to Alzheimer’s and Parkinson’s diseases.
Muschol, who recently received a three-year, $440,000 grant renewal from the National Institutes of Health to continue his work on the causes of Alzheimer’s, compares the concept of a CTE “seed” spreading within the damaged brain to “prion diseases,” a set of diseases in which damaged protein can transmit its damaged state to its healthy counterpart in the brain.
“Repeated concussions over many years may be the precursors of neurodegenerative diseases with amyloid formation, such as seen in Alzheimer’s,” said Muschol. “These head injuries may represent a singular event that disrupts cell function and allows the formation seeds for amyloid fibrils - misfolded proteins in the brain that self-assemble into crystal-like polymers. Once formed, these “seeds” could then slowly continue to self-replicate and spread in the brains of affected players who later develop CTE. Many more experiments will be required before such a potential correlation can be confirmed, however.”
According to Muschol, there are two ways that these “seeds” could spread in the brain.
“One way is by direct cell to cell transmission,” he explained. “Nerve cells in particular have long projections called ‘axons’ that connect them, so ‘seeds’ could be exchanged directly, cell to cell. They could also spread by diffusion in the vicinity of a diseased tissue.”
Both Alzheimer’s and Parkinson’s fall into the category of ‘amyloid diseases’ because they are caused by ‘amyloid fibrils’ forming in the brain. Muschol thinks that there are similar processes at work to cause CTE.
"We still don’t understand many aspects of amyloid formation, including the mechanisms by which amyloid formation induces cell death,” he explained. “ Surprisingly, it is not the loss of healthy proteins that is of major concern. Instead the protein aggregates themselves become toxic, causing cells and tissues to deteriorate and die.”
According to Muschol, what remains unclear are how often serious brain trauma, either from one event or multiple injuries over time, leads to CTE. He said it is also unknown whether a brain injury caused by a car crash, for example, or an improvised explosive device (IED), as often encountered by members of the military, could lead to CTE or something similar.
“There are reports that car crash victims with head injuries might develop amyloid deposits, at least temporarily,” said Muschol.
Because CTE was only recently identified it will likely take considerable research, not only to make links to other brain diseases and disorders, but also to learn more about the nature of CTE’s causes and symptoms.