Researchers at the University of Hong Kong have published the results of a study that identifies a potential new therapeutic target for epilepsy treatment. The research builds on recent findings regarding the role of neuroinflammation caused by abnormal reactive glial cells, including astrocytes and microglia, in temporal lobe epilepsy (TLE). This inflammation has been linked to connexin-based gap junctions and hemichannels in brain glial cells, with ongoing global research aiming to discover ways to block connexin hemichannels to reduce neuroinflammation with fewer side effects.
Discovery of D4 Compound
The Hong Kong research team identified a new small organic compound named D4, which selectively blocks connexin hemichannels without affecting gap junctions. In a mouse model, D4 was found to strongly suppress neuroinflammation-induced TLE, curb seizures, and increase survival rates. A single oral dose of D4 provided protection against further seizures.
Publication and Future Implications
The findings were published in the Proceedings of the National Academy of Sciences (PNAS) under the title “Inhibition of connexin hemichannels alleviates neuroinflammation and hyperexcitability in temporal lobe epilepsy.” The authors described the results as “exciting” evidence that targeting connexin hemichannels with D4 is an “effective and promising strategy for treating epilepsy where neuroinflammation plays a critical role.”-Fineline Info & Tech
