Epilepsy is one of the most common chronic diseases of the central nervous system (CNS).
Treatment of epilepsy remains, however, a clinical challenge with over 30% of patients not responding
to current pharmacological interventions. Complicating management of treatment, epilepsy comes
with multiple comorbidities, thereby further reducing the quality of life of patients. Increasing evidence
suggests purinergic signalling via extracellularly released ATP as shared pathological mechanisms
across numerous brain diseases. Once released, ATP activates specific purinergic receptors, including
the ionotropic P2X7 receptor (P2X7R). Among brain diseases, the P2X7R has attracted particular
attention as a therapeutic target. The P2X7R is an important driver of inflammation, and its activation
requires high levels of extracellular ATP to be reached under pathological conditions. Suggesting
the therapeutic potential of drugs targeting the P2X7R for epilepsy, P2X7R expression increases
following status epilepticus and during epilepsy, and P2X7R antagonism modulates seizure severity
and epilepsy development. P2X7R antagonism has, however, also been shown to be effective in treating
conditions most commonly associated with epilepsy such as psychiatric disorders and cognitive
deficits, which suggests that P2X7R antagonisms may provide benefits beyond seizure control. This
review summarizes the evidence suggesting drugs targeting the P2X7R as a novel treatment strategy
for epilepsy with a particular focus of its potential impact on epilepsy-associated comorbidities.
| Identifer | oai:union.ndltd.org:DRESDEN/oai:qucosa:de:qucosa:89164 |
| Date | 20 January 2024 |
| Creators | Gil, Beatriz, Smith, Jonathon, Tang, Yong, Illes, Peter, Engel, Tobias |
| Publisher | MDPI |
| Source Sets | Hochschulschriftenserver (HSSS) der SLUB Dresden |
| Language | English |
| Detected Language | English |
| Type | info:eu-repo/semantics/publishedVersion, doc-type:article, info:eu-repo/semantics/article, doc-type:Text |
| Rights | info:eu-repo/semantics/openAccess |
| Relation | 2380 |
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