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破解癫痫和阿尔茨海默病之间的新共享靶点:刻不容缓。

Cracking novel shared targets between epilepsy and Alzheimer's disease: need of the hour.

机构信息

Department of Pharmacology, Post Graduate Institute of Medical Education and Research, Chandigarh 1600142, Punjab, India.

Department of Pharmacology, Post Graduate Institute of Medical Education and Research, Chandigarh 1600142, Punjab, India, e-mail:

出版信息

Rev Neurosci. 2018 Jun 27;29(4):425-442. doi: 10.1515/revneuro-2017-0064.

Abstract

Epilepsy and Alzheimer's disease (AD) are interconnected. It is well known that seizures are linked with cognitive impairment, and there are various shared etiologies between epilepsy and AD. The connection between hyperexcitability of neurons and cognitive dysfunction in the progression of AD or epileptogenesis plays a vital role for improving selection of treatment for both diseases. Traditionally, seizures occur less frequently and in later stages of age in patients with AD which in turn implies that neurodegeneration causes seizures. The role of seizures in early stages of pathogenesis of AD is still an issue to be resolved. So, it is well timed to analyze the common pathways involved in pathophysiology of AD and epilepsy. The present review focuses on similar potential underlying mechanisms which may be related to the causes of seizures in epilepsy and cognitive impairment in AD. The proposed review will focus on many possible newer targets like abnormal expression of various enzymes like GSK-3β, PP2A, PKC, tau hyperphosphorylation, MMPs, caspases, neuroinflammation and oxidative stress associated with number of neurodegenerative diseases linked with epilepsy. The brief about the prospective line of treatment of both diseases will also be discussed in the present review.

摘要

癫痫和阿尔茨海默病(AD)是相互关联的。众所周知,癫痫发作与认知障碍有关,癫痫和 AD 之间存在多种共同的病因。神经元过度兴奋与 AD 或癫痫发生过程中的认知功能障碍之间的联系对于改善两种疾病的治疗选择起着至关重要的作用。传统上,AD 患者的癫痫发作频率较低,发生在老年后期,这反过来意味着神经退行性变引起癫痫发作。癫痫发作在 AD 发病早期的作用仍然是一个待解决的问题。因此,分析 AD 和癫痫的病理生理学中涉及的共同途径是适时的。本综述重点介绍了可能与癫痫发作和 AD 认知障碍的原因有关的相似潜在机制。拟议的综述将集中讨论许多可能的新靶点,如各种酶的异常表达,如 GSK-3β、PP2A、PKC、tau 过度磷酸化、MMPs、半胱天冬酶、神经炎症和氧化应激,这些与许多与癫痫相关的神经退行性疾病有关。本综述还将讨论两种疾病的潜在治疗方法。

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