Blocking receptor for advanced glycation end products (RAGE) or toll‐like receptor 4 (TLR4) prevents posttraumatic epileptogenesis in mice-Reference-Cited by-同舟云学术

Blocking receptor for advanced glycation end products (RAGE) or toll‐like receptor 4 (TLR4) prevents posttraumatic epileptogenesis in mice

Published:2021-09-18 Issue:12 Volume:62 Page:3105-3116
ISSN:0013-9580
Container-title:Epilepsia
language:en
Short-container-title:Epilepsia

Author:

Ping Xingjie¹²^ORCID,Chai Zhi³,Wang Weiping⁴,Ma Cungen³,White Fletcher A²⁵⁶,Jin Xiaoming¹²⁷^ORCID

Affiliation:

1. Department of Anatomy, Cell Biology and Physiology Indiana University School of Medicine Indianapolis Indiana USA

2. Spinal Cord and Brain Injury Research Group Stark Neurosciences Research InstituteIndiana University School of Medicine Indianapolis Indiana USA

3. Neurobiology Research Center Shanxi Key Laboratory of Innovative Drugs for Serious Illness College of Basic Medicine Shanxi University of Chinese Medicine Jinzhong China

4. Department of Neurology Affiliated Hangzhou First People's Hospital Zhejiang University School of Medicine Hangzhou China

5. Department of Anesthesia Indiana University School of Medicine Indianapolis Indiana USA

6. Research and Development Services Richard L. Roudebush VA Medical Center Indianapolis Indiana USA

7. Department of Neurological Surgery Indiana University School of Medicine Indianapolis Indiana USA

Funder

Citizens United for Research in Epilepsy

Publisher

Wiley

Subject

Clinical Neurology,Neurology

Link

https://onlinelibrary.wiley.com/doi/pdf/10.1111/epi.17069

Reference49 articles.

1. Epilepsy after head injury: An overview

2. Epilepsy after penetrating head injury. I. Clinical correlates: A report of the Vietnam Head Injury Study

3. Seizures after head trauma: A population study

4. Early and Late Posttraumatic Seizures in Traumatic Brain Injury Rehabilitation Patients: Brain Injury Factors Causing Late Seizures and Influence of Seizures on Long-Term Outcome

5. Epilepsy following cortical injury: Cellular and molecular mechanisms as targets for potential prophylaxis

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