Lithium Prevents Telomere Shortening in Cortical Neurons in Amyloid-Beta Induced Toxicity.

IF 1.6 Q3 CLINICAL NEUROLOGY

NeuroSci Pub Date : 2022-12-23 eCollection Date: 2023-03-01 DOI:10.3390/neurosci4010001

Rafael M Themoteo, Vanessa J R De Paula, Nicole K R Rocha, Helena Brentani, Orestes V Forlenza

{"title":"Lithium Prevents Telomere Shortening in Cortical Neurons in Amyloid-Beta Induced Toxicity.","authors":"Rafael M Themoteo, Vanessa J R De Paula, Nicole K R Rocha, Helena Brentani, Orestes V Forlenza","doi":"10.3390/neurosci4010001","DOIUrl":null,"url":null,"abstract":"Background: There is consistent evidence of the potential benefits of lithium attenuating mechanisms of neurodegeneration, including those related to the pathophysiology of Alzheimer's disease (AD), and facilitating neurotrophic and protective responses, including maintenance of telomere length. The aim was to investigate the protective effect of the pre-treatment with lithium on amyloid-beta (Aβ)-induced toxicity and telomere length in neurons.Methods: Cortical neurons were treated with lithium chloride at therapeutic and subtherapeutic concentrations (2 mM, 0.2 mM and 0.02 mM) for seven days. Amyloid toxicity was induced 24 h before the end of lithium treatment.Results: Lithium resulted in 120% (2 mM), 180% (0.2 mM) and 140% (0.02 mM) increments in telomere length as compared to untreated controls. Incubation with Aβ1-42 was associated with significant reductions in MTT uptake (33%) and telomere length (83%) as compared to controls.Conclusions: Lithium prevented loss of culture viability and telomere shortening in neuronal cultures challenged with Aβ fibrils.","PeriodicalId":74294,"journal":{"name":"NeuroSci","volume":"4 1","pages":"1-8"},"PeriodicalIF":1.6000,"publicationDate":"2022-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11523687/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"NeuroSci","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3390/neurosci4010001","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2023/3/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Background: There is consistent evidence of the potential benefits of lithium attenuating mechanisms of neurodegeneration, including those related to the pathophysiology of Alzheimer's disease (AD), and facilitating neurotrophic and protective responses, including maintenance of telomere length. The aim was to investigate the protective effect of the pre-treatment with lithium on amyloid-beta (Aβ)-induced toxicity and telomere length in neurons.

Methods: Cortical neurons were treated with lithium chloride at therapeutic and subtherapeutic concentrations (2 mM, 0.2 mM and 0.02 mM) for seven days. Amyloid toxicity was induced 24 h before the end of lithium treatment.

Results: Lithium resulted in 120% (2 mM), 180% (0.2 mM) and 140% (0.02 mM) increments in telomere length as compared to untreated controls. Incubation with Aβ_1-42 was associated with significant reductions in MTT uptake (33%) and telomere length (83%) as compared to controls.

Conclusions: Lithium prevented loss of culture viability and telomere shortening in neuronal cultures challenged with Aβ fibrils.

查看原文本刊更多论文

锂能防止淀粉样蛋白-β诱导毒性皮层神经元端粒缩短

背景：有一致的证据表明，锂可减轻神经退行性变的机制，包括与阿尔茨海默病（AD）病理生理学相关的机制，并促进神经营养和保护性反应，包括端粒长度的维持。目的是研究锂的预处理对淀粉样β（Aβ）诱导的毒性和神经元端粒长度的保护作用：用治疗浓度和亚治疗浓度（2 mM、0.2 mM 和 0.02 mM）的氯化锂处理皮层神经元七天。在锂治疗结束前 24 小时诱导淀粉样蛋白毒性：结果：与未处理的对照组相比，锂使端粒长度分别增加了120%（2 mM）、180%（0.2 mM）和140%（0.02 mM）。与对照组相比，用Aβ1-42孵育可显著降低MTT吸收率（33%）和端粒长度（83%）：结论：锂能防止神经元培养物在受到 Aβ 纤维挑战时丧失培养活力和端粒缩短。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

NeuroSci

自引率

0.00%

发文量

审稿时长

11 weeks