Epilepsy, inflammation and the onset of seizures

Epileptic seizures have been likened to a wildfire of excitation spreading through the brain. It will not surprise readers of these posts that two papers just published in the journal Nature Medicine describe a key role for inflammation in the onset of seizures. The first paper begins with a salient observation:

"Brain inflammation is a major factor in epilepsy, but the impact of specific inflammatory mediators on neuronal excitability is incompletely understood."

They proceed to describe how they...

"...discovered a proconvulsant pathway involving high-mobility group box-1 (HMGB1) release from neurons and glia and its interaction with Toll-like receptor 4 (TLR4), a key receptor of innate immunity."

The conclude by noting that inflammation associated with...

"HMGB1-TLR4 signaling may contribute to generating and perpetuating seizures in humans and might be targeted to attain anticonvulsant effects in epilepsies that are currently resistant to drugs."

The second paper published in the same journal celebrates the potential therapeutic benefit of an intervention that blocks pathways of inflammatory signaling:

"Blocking this inflammatory pathway may constitute a new antiepileptic treatment strategy."

You may also like to see an editorial in the journal Science Signaling entitled Inflamed About Epilepsy that summarizes these important findings.

"Together, these data suggest that the HMGB1-TLR4 pathway may underlie the onset of seizures and thus provide a new therapeutic strategy to target epilepsy."

The 'take home' message is that we have further evidence of the importance of the healthy regulation of inflammation as an indispensable element in your strategy for brain health.