Reduced Expression of Voltage-Gated Sodium Channel Beta 2 Restores Neuronal Injury and Improves Cognitive Dysfunction Induced by Aβ1-42. (10th November 2022)

• Record Type: Journal Article
• Authors: Li, Shan; Yan, Guo-Ji; Tan, Ya-Xin; Xue, Lu-Lu; Wang, Ting-Hua; Zhao, Hao-Ran; Lu, Min-Nan; Zhang, Hui-Xiang; Mei, Rong; Dong, Xiao-Han; Liu, Li-Na; Wang, Dan; Xiyang, Yan-Bin
• Other Names: Peña-Ortega Fernando Academic Editor.
• Is Part Of: Neural plasticity. Volume 2022(2022)
• Publication Date: 2022-11-10
• Subjects: Neuroplasticity -- Periodicals; 612.82
• DOI: 10.1155/2022/3995227
• Languages: English
• ISSNs: 2090-5904

Abstract

Abstract : Voltage-gated sodium channel beta 2 (Nav2.2 or Nav β 2, coded by SCN2B mRNA), a gene involved in maintaining normal physiological functions of the prefrontal cortex and hippocampus, might be associated with prefrontal cortex aging and memory decline. This study investigated the effects of Nav β 2 in amyloid- β 1-42- (A β 1-42-) induced neural injury model and the potential underlying molecular mechanism. The results showed that Nav β 2 knockdown restored neuronal viability of A β 1-42-induced injury in neurons; increased the contents of brain-derived neurotrophic factor (BDNF), enzyme neprilysin (NEP) protein, and NEP enzyme activity; and effectively altered the proportions of the amyloid precursor protein (APP) metabolites including A β 42, sAPP α, and sAPP β, thus ameliorating cognitive dysfunction. This may be achieved through regulating NEP transcription and APP metabolism, accelerating A β degradation, alleviating neuronal impairment, and regulating BDNF-related signal pathways to repair neuronal synaptic efficiency. This study provides novel evidence indicating that Nav β 2 plays crucial roles in the repair of neuronal injury induced by A β 1-42 both in vivo and in vitro .