Rafael M Themoteo, Vanessa J R De Paula, Nicole K R Rocha, Helena Brentani, Orestes V Forlenza
{"title":"锂能防止淀粉样蛋白-β诱导毒性皮层神经元端粒缩短","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":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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<sub>1-42</sub> was associated with significant reductions in MTT uptake (33%) and telomere length (83%) as compared to controls.</p><p><strong>Conclusions: </strong>Lithium prevented loss of culture viability and telomere shortening in neuronal cultures challenged with Aβ fibrils.</p>","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":"{\"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\":\"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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<sub>1-42</sub> was associated with significant reductions in MTT uptake (33%) and telomere length (83%) as compared to controls.</p><p><strong>Conclusions: </strong>Lithium prevented loss of culture viability and telomere shortening in neuronal cultures challenged with Aβ fibrils.</p>\",\"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}","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}
Lithium Prevents Telomere Shortening in Cortical Neurons in Amyloid-Beta Induced Toxicity.
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.
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