Stroke can leave a lifelong problem because neurons are damaged and die. But now, researchers at the University of Pittsburgh’s Brain Institute have identified a new drug that can help prevent injuries, even after a stroke, and tests in mice have shown promise. When a stroke occurs, blood vessels in the brain become clogged, blocking blood flow and causing the death of oxygen-deprived neurons. But neurons in the surrounding area can also be affected and may die after hours or days. And these are the focus of the new research.
“We’re also looking for ways to prevent these other neurons from dying,” said Elias Aizenman, senior author of the study. “If we can do this, recovery may improve, and we may be better able to help stroke patients, where blood clots are in inaccessible blood vessels, or in time for early intervention in hospitals.” With the right drugs, we may also be able to slow down the progression of a known stroke before a patient arrives at the hospital. “
Now researchers have developed an experimental new drug that can do just that. The new study builds on the team’s early work, and they found a mechanism that triggers cell death. Previously, the team had found that neurons die from the release of potassium ions from a potassium channel called Kv2.1. This can be triggered by the interaction between the channel and a protein called syntaxin. The researchers found that they could prevent cell death by interfering with this interaction by using a compound called TAT-C1aB.
In the new study, the team found a potential way to use the findings to further reduce cell death after stroke. They found that there are two types of Kv2.1 channels on the neuronal membranes, one of which helps the extra Kv2.1 channel find access to cells. This, in turn, increases the amount of potassium lost, and therefore increases cell death.
To deal with this, the team developed a small protein called TAT-DP-2. This prevents new channels from entering the cells, prevents potassium leakage and keeps the cells active. In tests on mice, the team found that animals that received TAT-DP-2 injections had a much smaller area of brain damage after a stroke than untreated mice. Treated mice also had better long-term nerve function.
The study seems promising, but like anything, there is no guarantee that the results will extend from mice to humans. Future work will need to see if this is feasible, but the ultimate hope is that a drug can eventually be administered even after a stroke to reduce damage and improve rehabilitation.
“There are no drugs in clinical practice that block cell death seleaguelifatal after stroke,” said Anthony Schulien, lead author of the study. “These trials provide exciting, early evidence of drug targeting, and we hope to one day translate it into patients. “
The study was published in the journal Science Advances.