A new study from Georgetown University Medical Center suggests that clearing aging support cells from the brain can significantly reduce epileptic seizures and improve memory, offering a potential new therapeutic pathway for drug-resistant epilepsy.
Temporal lobe epilepsy (TLE) is the most common form of epilepsy that fails to respond adequately to medication, affecting nearly 40% of people living with the disorder. In addition to recurrent seizures, TLE is frequently associated with memory loss and cognitive decline. Despite available treatments, a substantial proportion of patients continue to experience uncontrolled symptoms, highlighting the need for alternative approaches.
The study links TLE to the premature aging of glial cells, which play a critical role in supporting and protecting neurons. Examination of donated human brain tissue from epilepsy patients revealed a five-fold increase in senescent glial cells compared with tissue from individuals without epilepsy. These aging cells are known to release inflammatory signals that can disrupt normal brain function.
To further investigate this mechanism, researchers used a mouse model that mimics temporal lobe epilepsy. Within two weeks of the brain injury that triggered epilepsy, the mice showed marked increases in molecular markers of cellular aging. When the senescent cells were selectively removed, seizure activity decreased substantially, and cognitive performance improved.
Treatment led to an approximate 50% reduction in senescent cells, fewer seizures, and restored performance in maze-based memory tests. Notably, about one-third of the treated animals did not develop epilepsy at all, suggesting a protective effect when intervention occurs early.
The aging cells were eliminated using a combination of dasatinib, an FDA-approved drug for leukemia, and quercetin, a naturally occurring plant flavonoid with antioxidant and anti-inflammatory properties. This drug pairing has been widely studied in animal models of aging and age-related diseases, increasing confidence in its translational potential.
Because both compounds already have established safety profiles, the findings raise the possibility of faster progression toward clinical trials in humans. Researchers describe this approach as senotherapy, a strategy aimed at targeting and removing senescent cells to restore tissue function.
Beyond epilepsy, the results may have broader implications for understanding brain aging and neurodegenerative conditions such as Alzheimer’s disease, where glial cell dysfunction has also been implicated.
The NIH-funded study was published in Annals of Neurology and provides new insight into how targeting cellular aging processes could transform treatment strategies for neurological disorders