Since neurotoxicity of aluminium (Al) resembles the progressive neurodegeneration observed in Alzheimer Disease (AD), Al administration in several ways has been used to produce AD model. Intraperitoneal (ip) low dose (4.2 mg/ kg) Al injection in rats for long periods is the preferred method by some researchers. In this paper, the efficiency of this method for producing an AD model was evaluated. In this study, we looked at the neuropathology of Al and the characteristic lesions of AD by histological and immunohistochemical techniques and determined oxidative stress markers in the brains of Al-treated and control rats. We also made electrophysiological recordings at the hippocampus and evaluated possible behavioural changes by Morris water maze test. However, no pathologic changes occurred in the animals except for an impairment in long-term potentiation (LTP) in the hippocampus (e.g. the LTPs of population spike (PS) amplitude at 15 min post-tetanus were measured as 217±27% in Al-treated rats and as 240±42% in sham-treated rats, of baseline PS amplitude). According to the findings of the present study, low dose of ip Al in rats is not sufficient to produce a good AD model. Higher doses (≥10 mg/kg) should be used.

中文翻译：

---

大鼠低剂量铝的腹膜内给药：产生阿尔茨海默氏病模型有多好。

由于铝（Al）的神经毒性类似于在阿尔茨海默病（AD）中观察到的进行性神经变性，因此已通过多种方式使用Al来产生AD模型。长期向大鼠腹膜内（ip）低剂量（4.2 mg / kg）Al注射是一些研究人员的首选方法。在本文中，评估了该方法用于生成AD模型的效率。在这项研究中，我们通过组织学和免疫组化技术研究了Al的神经病理学和AD的特征性病变，并确定了Al治疗和对照大鼠大脑中的氧化应激标志物。我们还制作了海马的电生理记录，并通过莫里斯水迷宫测试评估了可能的行为变化。然而，除海马的长期增强作用（LTP）受损外，其他动物均未发生任何病理变化（例如，在经铝治疗的情况下，在破伤风后15分钟测得的种群峰值（PS）振幅的LTP为217±27％）大鼠和假治疗大鼠的240±42％（基线PS幅度）。根据本研究的发现，在大鼠中低剂量的ip A1不足以产生良好的AD模型。应使用更高剂量（≥10mg / kg）。