'Mini-brain' Model Explores Concussion's Effects at Cellular Level

By Bio-IT World Staff 

April 9, 2026 | A biomedical engineering professor at the University of Cincinnati is using studying how cells in the brain are affected by concussive forces—and how this trauma can lead to neurodegenerative diseases. 

Concussions are responsible for as many as 3 million emergency room visits every year. Children playing sports or other recreation activities sustain nearly 4 million concussions every year, according to estimates by the Centers for Disease Control and Prevention. UC College of Engineering and Applied Science Assistant Professor Volha “Olga” Liaudanskaya wants to know more about the milder, repetitive blows children in youth sports can sustain that can also lead to injury.  

"We still know very little about what’s going on in the brain. And the injury can depend on the severity and location,” she said in a press release. “Brain trauma is so different from patient to patient, both the intensity of the injury and the patients themselves.” 

Liaudanskaya said children are potentially exposed to mild brain injuries more often than we know. 

“So we wanted to understand what mild injuries do to the brain. Is there a threshold? Is it an accumulation? Can we heal it? What causes long-term neurodegeneration that is common in boxers and American football players,” she said, noting that these are key questions in TBI research. 

Building Mini Brains  

Liaudanskaya and her team are studying traumatic brain injury (TBI) at the cellular level using “mini-brains”. Assembloids are engineered fusions of region, cell, and lineage-specific tissues, she writes in a paper published last month in Frontiers in Cellular Neuroscience (DOI: /10.3389/fncel.2026.1787173). Liaudanskaya’s group combines three brain cell types that regulate brain activity, including neurons, with two vascular cells, creating a complex “pentaculture” of five cell types that she can track simultaneously using living tissue. 

“For neurodegenerative diseases, the vascular system is a critical driver of inflammation, degeneration and proteinopathies like Alzheimer’s, Parkinson’s and chronic traumatic encephalopathy or CTE,” she said. For people with a history of concussions or repeated blunt-force head trauma, understanding this vascular contribution is especially important.  

Liaudanskaya is also examining how mitochondria are affected and react to these concussive forces. “The mitochondria plays a big role in neurodegeneration,” she said. The team tagged mitochondria in neurons with a red fluorescent protein, astrocytic mitochondria with green tags, and microglial mitochondria with white tags. The fluorescent tags let researchers watch the mitochondria migrate in the cell as the researchers subject the cells to concussive-like forces with mechanical devices that allow for consistent, measurable and replicable forces across samples, simulating blunt-force trauma that can cause concussions and traumatic brain injury. 

Liaudanskaya found that in injured brain cells, certain proteins that normally stabilize neurons fail to return to their normal function. Fibers between nerve cells break down. There is chronic inflammation and metabolic dysfunction. And these are hallmarks of neurodegenerative disease. 

Still, most people with concussions fully recover given enough time and the absence of any additional traumatic blows, she said. “If you protect your brain for six months, you can recover. We see a pattern develop in the third month. Everything is stabilizing at the structural level, but you still have inflammation. If you extend it to six months and have another concussion, you start over,” she said.