Themoteo Rafael M, De Paula Vanessa J R, Rocha Nicole K R, Brentani Helena, Forlenza Orestes V
Laboratory of Neuroscience (LIM-27), Departamento e Instituto de Psiquiatria, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de São Paulo, Sao Paulo 05508-090, SP, Brazil.
Laboratory of Psychobiology (LIM-23), Instituto de Psiquiatria, Hospital das Clinicas HCFMUSP, Faculdade de Medicina, Universidade de São Paulo, Sao Paulo 05508-090, SP, Brazil.
NeuroSci. 2022 Dec 23;4(1):1-8. doi: 10.3390/neurosci4010001. eCollection 2023 Mar.
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.
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.
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 was associated with significant reductions in MTT uptake (33%) and telomere length (83%) as compared to controls.
Lithium prevented loss of culture viability and telomere shortening in neuronal cultures challenged with Aβ fibrils.
有一致的证据表明锂具有潜在益处，可减弱神经退行性变机制，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反应，包括维持端粒长度。目的是研究锂预处理对淀粉样β蛋白（Aβ）诱导的神经元毒性和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）的氯化锂处理皮质神经元7天。在锂治疗结束前24小时诱导淀粉样毒性。
与未处理的对照组相比，锂使端粒长度增加了120%（2 mM）、180%（0.2 mM）和140%（0.02 mM）。与对照组相比，用Aβ孵育导致MTT摄取显著降低（33%）和端粒长度显著缩短（83%）。
锂可防止用Aβ原纤维攻击的神经元培养物中培养活力的丧失和端粒缩短。
