Building the Case Against Inflammation
An earlier study by two of the team’s scientists showed that when a protein called albumin is able to make it through the blood-brain barrier, it sparks an inflammatory response that damages nerve cells and makes them function abnormally. The current study showed that, at least in mice, the introduction of albumin into the brain produces effects that look much like the negative effects of aging. Among other things, the albumin-affected mice were not able to find their way through a maze as well as young, healthy mice could.
Even more hopeful is the study’s finding that when the mice were given a drug that blocked the effects of albumin, their brains began to look young again. They were less prone to seizures, and they were able to navigate a maze as well as a young mouse.
The team was not, at first, trying to find a way to turn back the clock on the brain’s aging process. But their investigation into problems with the blood-brain barrier may have inadvertently uncovered a new hope for dementia patients.
“We got to this through this back door; we started with questions about plasticity having to do with the blood-brain barrier, traumatic brain injury and how epilepsy develops,” Kaufer said. “But after we’d learned a lot about the mechanisms, we started thinking that maybe in aging it is the same story. This is new biology, a completely new angle on why neurological function deteriorates as the brain ages.”
UC Berkeley, Drugs that quell brain inflammation reverse dementia
Science Translational Medicine, Blood-brain barrier dysfunction in aging induces hyperactivation of TGFβ signaling and chronic yet reversible neural dysfunction