Neuropharmacology Research Laboratory, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Jalan Lagoon Selatan, Bandar Sunway, Selangor, Malaysia.
Neuropharmacology Research Laboratory, Jeffrey Cheah School of Medicine and Health Sciences, Monash University Malaysia, Jalan Lagoon Selatan, Bandar Sunway, Selangor, Malaysia.
Eur J Pharmacol. 2018 Oct 15;837:145-155. doi: 10.1016/j.ejphar.2018.08.020. Epub 2018 Aug 17.
Epilepsy is a devastating condition affecting around 70 million people worldwide. Moreover, the quality of life of people with epilepsy (PWE) is worsened by a series of comorbidities. The neurobehavioral comorbidities discussed herein share a reciprocal and complex relationship with epilepsy, which ultimately complicates the treatment process in PWE. Understanding the mechanistic pathway by which these comorbidities are associated with epilepsy might be instrumental in developing therapeutic interventions. Inflammatory cytokine signaling in the brain regulates important brain functions including neurotransmitter metabolism, neuroendocrine function, synaptic plasticity, dopaminergic transmission, the kynurenine pathway, and affects neurogenesis as well as the neural circuitry of moods. In this review, we hypothesize that the complex relationship between epilepsy and its related comorbidities (cognitive impairment, depression, anxiety, autism, and schizophrenia) can be unraveled through the inflammatory mechanism that plays a prominent role in all these individual conditions. An ample amount of evidence is available reporting the role of inflammation in epilepsy and all individual comorbid condition but their complex relationship with epilepsy has not yet been explored through the prospective of inflammatory pathway. Our review suggests that epilepsy and its neurobehavioral comorbidities are associated with elevated levels of several key inflammatory markers. This review also sheds light on the mechanistic association between epilepsy and its neurobehavioral comorbidities. Moreover, we analyzed several anti-inflammatory therapies available for epilepsy and its neurobehavioral comorbidities. We suggest, these anti-inflammatory therapies might be a possible intervention and could be a promising strategy for preventing epileptogenesis and its related neurobehavioral comorbidities.
癫痫是一种全球性疾病，影响着全球约 7000 万人。此外，癫痫患者（PWE）的生活质量因一系列合并症而恶化。本文讨论的神经行为合并症与癫痫存在相互复杂的关系，这最终使 PWE 的治疗过程复杂化。了解这些合并症与癫痫相关的机制途径可能有助于开发治疗干预措施。大脑中的炎症细胞因子信号转导调节着重要的大脑功能，包括神经递质代谢、神经内分泌功能、突触可塑性、多巴胺能传递、犬尿氨酸途径，并影响神经发生以及情绪的神经回路。在这篇综述中，我们假设通过在所有这些疾病中都发挥重要作用的炎症机制，可以揭示癫痫及其相关合并症（认知障碍、抑郁、焦虑、自闭症和精神分裂症）之间的复杂关系。有大量证据表明炎症在癫痫和所有单独的合并症中都发挥作用，但它们与癫痫之间的复杂关系尚未通过炎症途径来探讨。我们的综述表明，癫痫及其神经行为合并症与几种关键炎症标志物的水平升高有关。这篇综述还阐明了癫痫与其神经行为合并症之间的机制关联。此外，我们分析了几种针对癫痫及其神经行为合并症的抗炎治疗方法。我们认为，这些抗炎治疗方法可能是一种可行的干预措施，并可能成为预防癫痫发生及其相关神经行为合并症的有前途的策略。
