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精神分裂症起源于过量γ-氨基丁酸(GABA)和突触修剪的可能机制。

Possible mechanism of schizophrenia origin by excess GABA and synaptic pruning.

作者信息

Rabinovitch A, Braunstein D, Rabinovitch R, Biton Y

机构信息

Physics Dept. Ben-Gurion University, Beer-Sheva, Israel.

Physics Dept. Sami Shamoon College of Engineering, Beer-Sheva, Israel.

出版信息

IBRO Neurosci Rep. 2023 Jul 28;15:126-130. doi: 10.1016/j.ibneur.2023.07.005. eCollection 2023 Dec.

Abstract

Schizophrenia is a psychotic disorder that affects approximately 1% of the global population. However, the etiology of this illness remains a subject of debate. One of the proposed mechanisms underlying schizophrenia is the synaptic pruning mediated by microglia in the brains of individuals with schizophrenia, although the precise mechanisms of this process remain elusive. In this regard, we propose that the potential development of the disease stems from both a genetic predisposition leading to an excessive production of GABAergic neurons and an exaggerated effort to maintain the E/I (excitation/inhibition) balance in the brain.

摘要

精神分裂症是一种精神病性障碍,影响着全球约1%的人口。然而,这种疾病的病因仍然是一个有争议的话题。尽管精神分裂症患者大脑中由小胶质细胞介导的突触修剪的确切机制仍不清楚,但这一过程被认为是精神分裂症潜在的发病机制之一。在这方面,我们认为该疾病的潜在发展源于两个方面:一是导致GABA能神经元过度产生的遗传易感性,二是大脑中维持兴奋/抑制(E/I)平衡的过度努力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6d64/10415689/b426da814010/gr1.jpg

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