Lab-grown 'minibrains' help reveal why traumatic brain injury raises dementia risk

Minibrains grown in the lab may help explain why concussions and other traumatic brain injuries (TBIs) raise people's risk of dementia.

In a new study, published Thursday (April 4) in the journal Cell Stem Cell, scientists reported the results of an experiment in which they blasted these lab-grown models of the human brain — known as cerebral organoids — with high-intensity ultrasonic waves. The waves were intended to mimic damage to brain cells induced by severe traumatic brain injuries.

The research hints at a strategy to block the downstream effects of brain injuries, the study authors reported. In theory, the treatment could be used as either a preventive measure or a therapy given post-injury. However, many more studies are needed before such a treatment could be used in people.

The cerebral organoids used in the study looked like pinhead-sized clumps of brain cells, rather than perfectly miniaturized versions of full-size human brains. That said, organoids capture aspects of human biology that are difficult to study in Animals, like lab mice. They can also be grown to include specific types of cells from different regions of the brain, arranged in layers as they would be in a person's head.

Related: Even mild concussions can 'rewire' the brain, possibly causing long-term symptoms

In this study, the researchers grew the organoids from cells collected from Healthy human donors and from people with either amyotrophic lateral sclerosis (ALS) or frontotemporal dementia, two types of neurodegenerative disease. Scientists have found that mutations in a gene called C9orf72 raise the risk of both diseases, and in this case, all of the donors carried a mutant copy of that gene.

The cells collected from each group were tweaked in the lab so they reverted into stem cells that could then be coaxed to grow into any type of cell. The researchers blasted the resulting organoids with ultrasonic pulses to mimic some effects of a TBI, including brain cell death and changes in a protein called tau, which is implicated in Alzheimer's disease.