The increase of amyloid beta (Aβ) release and hyperphosphorylation of Tau protein represents the main events related to Alzheimer’s disease (AD). Furthermore, the sporadic type represents the most common form of AD. Therefore, the establishment of a non-transgenic animal model that resembles the characteristics of the disease is of particular importance. Scopolamine has been linked to increases in both Aβ production and oxidative stress in rat and mice brains. Thus, the purpose of the present work was to identify changes in biomarkers that are related to AD after chronic administration of scopolamine (2 mg/kg i.p., during 6 and 12 weeks) to male Wistar rats. The results showed increased Aβ deposition at rat hippocampus which could be due to an increase of β-site amyloid-β-protein precursor cleaving enzyme 1 (BACE1) expression and activity. These findings could be related to the increase of glycogen synthase kinase 3 phosphorylated (GSK3βP9) expression. Finally, the establishment of a state of oxidative stress in groups treated with scopolamine was demonstrated by an increase in free radical content and MDA levels. The present study facilitates our understanding of the changes that occur in biomolecules related to AD in Wistar rats after the chronic administration of scopolamine.

淀粉样蛋白β（Aβ）释放的增加和Tau蛋白的过度磷酸化代表了与阿尔茨海默病（AD）相关的主要事件。此外，偶发类型代表AD的最常见形式。因此，建立类似于该疾病特征的非转基因动物模型特别重要。东pol碱与大鼠和小鼠大脑中Aβ的产生和氧化应激的增加有关。因此，本研究的目的是确定向雄性Wistar大鼠长期施用东pol碱（2 mg / kg ip，6和12周）后与AD相关的生物标志物变化。结果表明，大鼠海马区Aβ沉积增加，这可能是由于β位淀粉样β蛋白前体裂解酶1（BACE1）的表达和活性增加所致。这些发现可能与糖原合酶激酶3磷酸化（GSK3βP9）表达增加有关。最后，通过东pol碱治疗的组中自由基含量和MDA含量的增加证明了氧化应激状态的建立。本研究有助于我们了解东pol碱长期给药后Wistar大鼠与AD相关的生物分子中发生的变化。