Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER), Ahmedabad, Gandhinagar, Gujarat, India.
Cellular and Molecular Neurobiology Laboratory, Department of Life Science and Bioinformatics, Assam University, Silchar, Assam, India.
Curr Top Med Chem. 2020;20(13):1154-1168. doi: 10.2174/1568026620666200416090820.
The occurrence of secondary neurodegeneration has exclusively been observed after the first incidence of stroke. In humans and rodents, post-stroke secondary neurodegeneration (SND) is an inevitable event that can lead to progressive neuronal loss at a region distant to initial infarct. SND can lead to cognitive and motor function impairment, finally causing dementia. The exact pathophysiology of the event is yet to be explored. It is seen that the thalami, in particular, are susceptible to cause SND. The reason behind this is because the thalamus functioning as the relay center and is positioned as an interlocked structure with direct synaptic signaling connection with the cortex. As SND proceeds, accumulation of misfolded proteins and microglial activation are seen in the thalamus. This leads to increased neuronal loss and worsening of functional and cognitive impairment.
There is a necessity of specific interventions to prevent post-stroke SND, which are not properly investigated to date owing to sparsely reproducible pre-clinical and clinical data. The basis of this review is to investigate about post-stroke SND and its updated treatment approaches carefully.
Our article presents a detailed survey of advances in studies on stroke-induced secondary neurodegeneration (SND) and its treatment.
This article aims to put forward the pathophysiology of SND. We have also tabulated the latest treatment approaches along with different neuroimaging systems that will be helpful for future reference to explore.
In this article, we have reviewed the available reports on SND pathophysiology, detection techniques, and possible treatment modalities that have not been attempted to date.
继发性神经退行性变仅在首次中风后发生。在人类和啮齿动物中，中风后继发性神经退行性变（SND）是一种不可避免的事件，可导致初始梗死灶远处的神经元进行性丧失。SND 可导致认知和运动功能障碍，最终导致痴呆。该事件的确切病理生理学尚未被探索。可以看到，特别是丘脑，容易引起 SND。背后的原因是丘脑作为中继中心，与大脑皮层直接通过突触信号连接，形成联锁结构。随着 SND 的进展，在丘脑内可以看到错误折叠蛋白的积累和小胶质细胞的激活。这导致神经元丢失增加，功能和认知障碍恶化。
需要有针对 SND 的特定干预措施，但迄今为止，由于临床前和临床数据的重复性较差，这些干预措施尚未得到充分研究。本综述的基础是仔细研究中风后 SND 及其更新的治疗方法。
我们的文章详细调查了关于中风诱导的继发性神经退行性变（SND）及其治疗的研究进展。
本文旨在提出 SND 的病理生理学。我们还列出了最新的治疗方法以及不同的神经影像学系统，这将有助于未来的研究。
在本文中，我们回顾了关于 SND 病理生理学、检测技术和可能的治疗方法的现有报告，这些方法迄今为止尚未尝试过。
