中国神经再生研究(英文版) ›› 2024, Vol. 19 ›› Issue (9): 1865-1866.doi: 10.4103/1673-5374.390975

• 观点:脑损伤修复保护与再生 • 上一篇    下一篇

Nrf2作为治疗癫痫的潜在靶点

  

  • 出版日期:2024-09-15 发布日期:2024-01-25

Nrf2 as a potential target for the treatment of epilepsy

Prince Kumar Singh, Tawfeeq Shekh-Ahmad*#br#   

  1. Institute for Drug Research, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel
  • Online:2024-09-15 Published:2024-01-25
  • Contact: Tawfeeq Shekh-Ahmad, PhD, Tawfeeq.Shekh-Ahmad@mail.huji.ac.il.
  • Supported by:
    This work was supported by The Israel Science Foundation, No. 1976/20 (to TSA).

摘要: https://orcid.org/0000-0002-6165-2219 (Tawfeeq Shekh-Ahmad)

Abstract: Epilepsy is a prevalent chronic brain disorder that is characterized by a persistent predisposition to recurrently generate epileptic seizures and is often associated with cognitive and psychological consequences. Epilepsy affects approximately 65 million individuals, including both males and females of all ages worldwide, and poses a significant burden on patients, their families, and the health system (Vezzani et al., 2019). Although a substantial number of anti-seizure medications have been approved by the FDA for the treatment of epilepsy, these therapies fail to prevent the development of seizures or permanently halt the occurrence of chronic disease (Glauser et al., 2013), and more than 30% of patients with epilepsy remain resistant to these medications and endure recurrent spontaneous seizures.  Therefore, the search for alternative therapeutic targets with anti-epileptogenic and anti-seizure potential could offer a promising avenue for addressing the challenges related to drug-resistant epilepsy treatment. Drug resistance is a particular challenge in patients with temporal lobe epilepsy, in which seizures originate mostly in the hippocampus, and many of these cases are acquired and arise following brain insults, such as prolonged seizures, traumatic brain injuries, or strokes. Several studies have confirmed that oxidative stress (OS) and elevated levels of reactive oxygen species (ROS) play crucial roles in the development and progression of epilepsy following such brain injuries.