A study of the brains of deceased headbutting animals has revealed, for the first time, similar enough hallmarks to human traumatic brain injury (TBI) to warrant further research of these big animals as future TBI models.
Currently, most TBI research is undertaken using the very common mouse model. Biologically, humans and mice are very similar, sharing over 70 percent of their genes, and housing the same organs. That’s why mice make an excellent medical model 99 percent of the time. However, when it comes to brains, mice and humans have one glaring different—a rodent’s brain is smooth, while a human’s is folded. On the other hand, bovids—such as cows, buffalo and the muskoxen and bighorn sheep used in this study—have the same folded brains that are seen in humans.
In the experimental study published in Acta Neuropathologica, Nicole Ackermans, postdoctoral fellow at Mount Sinai Hospital (New York), and colleagues examined the brains of three deceased muskoxen from Greenland and four bighorn sheep, from parks in Colorado and Utah and the Buffalo Zoo.
The researchers chose to focus their study on these horned animals specifically as they are known to engage in violent head-to-head collisions, with male muskoxen often reaching speeds of up to 30 mph before impact.
According to the researchers, at first glance, the animals’ brains looked healthy and brain scans showed that the overall structure of each animal’s brain was intact. However, that changes once the team sliced into the individual brains.
To look for signs of TBI damage, the researchers treated thin slices of the animals’ brains with antibodies made to detect phosphorylated tau proteins found in humans and/or mice. This form of tau is a hallmark of damage often seen in the brains of Alzheimer’s disease patients as well as those who have suffered TBIs, including chronic traumatic encephalopathy (CTE).
Under a microscope, the researchers discovered that one of the antibodies stained muskoxen brains at easily detectable levels, whereas a different antibody stained bighorn sheep brains at only lightly detectable levels. Additionally, the prefrontal cortex of the muskoxen brains had high levels of tau protein tangles near the surface of the cortex—another hallmark of CTE.
“At first, we were surprised [by the results],” said Ackermans. “One of the challenges with these kinds of studies is that we don’t know whether antibodies used on human and rodents will work on bovid brains. The fact that we detected these antibodies was important. It suggested that the brains of these animals, especially the muskoxen, sustain TBI-like damage.”
While the tau distribution pattern is similar to that seen in mild TBI and early-stage CTE cases, it differs from what is seen in Alzheimer’s disease patients. Those patients typically present with a well-defined bilaminar pattern.
In humans, a single TBI leads to a high chance of developing neurodegenerative diseases, and chronic TBI only increases those chances. Meanwhile, muskoxen and bighorn sheep are known to headbutt every year during the 4-month rut from July to October. A low estimate of three fights per week during the rut, with five clashes each, leads to about 210 clashes per year at around 60 km/h, averaging 2,100 clashes in a lifetime. In comparison, studies on professional football players recorded a median number of 250 impacts per season at around 20 km/h, similarly averaging 2,000 clashes in a lifetime for an average career of 8 years.
“The muskoxen’s capacity to survive yearly, repetitive, brain trauma and their similar frequency in this behavior to high-risk TBI individuals, like football players and war veterans, presents them and likely other bovids as a model with enough similarities to human CTE to explore the natural development of TBI,” write the scientists in their paper. The authors even specifically point to the headbutting bovids “as a model for sports-related TBI.”