ABA补充挽救阿尔茨海默病三重转基因小鼠模型中IRS2和BDNF mRNA水平。

IF 2.8 Q2 NEUROSCIENCES Journal of Alzheimer's disease reports Pub Date : 2023-09-08 eCollection Date: 2023-01-01 DOI:10.3233/ADR-230056
Laryssa Alves-Borba, Verónica Espinosa-Fernández, Ania Canseco-Rodríguez, Ana María Sánchez-Pérez
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引用次数: 0

摘要

胰岛素抵抗通过影响神经炎症和脑源性神经营养因子(BDNF)的表达而成为阿尔茨海默病(AD)的基础。在此,我们评估了早期和晚期脱落酸(ABA)干预对AD三重转基因小鼠模型中海马BDNF、肿瘤坏死因子α(TNFα)和胰岛素受体底物(IRS)1/2 mRNA水平的影响。与野生型小鼠相比,转基因小鼠表现出较低的BDNF和IRS2,相等的IRS1,以及较高的TNFα表达。晚期ABA处理可以挽救TNFα并增加IRS1/2的表达。然而,早期给予ABA是增加BDNF表达所必需的。我们的数据表明,ABA的早期干预可以通过挽救IRS1/2和BDNF的表达来预防AD。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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ABA Supplementation Rescues IRS2 and BDNF mRNA Levels in a Triple-Transgenic Mice Model of Alzheimer's Disease.

Insulin resistance underlies Alzheimer's disease (AD) by affecting neuroinflammation and brain-derived neurotrophic factor (BDNF) expression. Here, we evaluated the effect of early and late-start abscisic acid (ABA) intervention on hippocampal BDNF, tumor necrosis factor α (TNFα), and insulin receptors substrates (IRS) 1/2 mRNA levels in a triple-transgenic mice model of AD. Transgenic mice displayed lower BDNF and IRS2, equal IRS1, and higher TNFα expression compared to wild-type mice. Late ABA treatment could rescue TNFα and increased IRS1/2 expression. However, early ABA administration was required to increase BDNF expression. Our data suggests that early intervention with ABA can prevent AD, via rescuing IRS1/2 and BDNF expression.

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