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脑可塑性障碍作为痴呆治疗和预防的潜在治疗靶点。

Impaired brain plasticity as a potential therapeutic target for treatment and prevention of dementia.

机构信息

a Centre for Addiction and Mental Health and Department of Psychiatry , University of Toronto , Toronto , ON , Canada.

出版信息

Expert Opin Ther Targets. 2019 Jan;23(1):21-28. doi: 10.1080/14728222.2019.1550074. Epub 2018 Nov 30.

Abstract

In 2017, it was estimated that close to 50 million people were living with dementia worldwide and this number is expected to double every 20 years. No effective treatment exists yet probably because by the time Alzheimer's dementia (AD) has developed it is too late to intervene. Areas covered: Mild cognitive impairment (MCI) is a clinical state that typically precedes AD. In MCI, the prefrontal cortex supports compensatory mechanisms that depend on robust synaptic plasticity and that delay progression to AD. This review focuses on novel neurostimulation approaches that could enhance prefrontal cortical plasticity in vivo by enhancing prefrontal cortical plasticity and function in patients with MCI or AD. It also describes novel neurophysiological markers that could function as targets for such approaches. Expert commentary: Targeting synaptic plasticity in patients with early AD or at risk of developing AD could be a promising approach to slow progression or prevent AD.

摘要

2017 年,据估计,全球有近 5000 万人患有痴呆症,预计这一数字每 20 年将翻一番。目前还没有有效的治疗方法,可能是因为当阿尔茨海默病(AD)发展时,进行干预为时已晚。

涵盖领域

轻度认知障碍(MCI)是一种临床状态,通常先于 AD。在 MCI 中,前额叶皮层支持补偿机制,这些机制依赖于强大的突触可塑性,并延迟向 AD 的进展。

本综述重点介绍了新的神经刺激方法,这些方法可以通过增强 MCI 或 AD 患者的前额叶皮层可塑性和功能,在体内增强前额叶皮层可塑性。它还描述了可作为此类方法目标的新型神经生理学标志物。

专家评论

针对早期 AD 患者或有发展 AD 风险的患者的突触可塑性可能是减缓进展或预防 AD 的有前途的方法。

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