The compelling role of allopurinol in hyperuricemia-induced epilepsy: Unrecognized like tears in rain

Ali Abdullah AlAseeri, Hayder M. Al-kuraishy, Ali I. Al-Gareeb, Naif H. Ali, Athanasios Alexiou, Marios Papadakis, Mostafa M. Bahaa, Mubarak Alruwaili, Gaber El Saber Batiha

Research output: Contribution to journalReview articlepeer-review

5 Scopus citations

Abstract

Epilepsy is a common neurological disease characterized by the recurrent, paroxysmal, and unprovoked seizures. It has been shown that hyperuricemia enhances and associated with the development and progression of epilepsy through induction of inflammation and oxidative stress. In addition, uric acid is released within the brain and contributes in the development of neuronal hyperexcitability and epileptic seizure. Brain uric acid acts as damage associated molecular pattern (DAMP) activates the immune response and induce the development of neuroinflammation. Therefore, inhibition of xanthine oxidase by allopurinol may reduce hyperuricemia-induced epileptic seizure and associated oxidative stress and inflammation. However, the underlying mechanism of allopurinol in the epilepsy was not fully elucidated. Therefore, this review aims to revise from published articles the link between hyperuricemia and epilepsy, and how allopurinol inhibits the development of epileptic seizure.

Original languageEnglish
Article number110973
JournalBrain Research Bulletin
Volume213
DOIs
StatePublished - Jul 2024

Keywords

  • Allopurinol
  • Epilepsy
  • Inflammation
  • Oxidative stress

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