Zaman Fashami Maryam, Bajelan Aida, Shakur Hamidreza, Khakpai Fatemeh, Rouhollah Fatemeh, Vaseghi Salar, Ghorbani Yekta Batool
Department of Physiology, Faculty of Medicine, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Department of Cellular and Molecular Sciences, Faculty of Advanced Sciences and Technology, Tehran University of Medical Sciences, Islamic Azad University, Tehran, Iran.
Biol Trace Elem Res. 2024 Dec 7. doi: 10.1007/s12011-024-04474-0.
Alzheimer's disease (AD) is one of the most common neurodegenerative disorders, characterized by the slow and progressive loss of brain structure and function, primarily affecting older individuals. Evidence has shown that disruption of zinc homeostasis in the brain contributes to synaptic dysfunction, as well as impairments in learning and memory. In this study, we evaluated the effect of zeolite zinc on memory performance and hippocampal cell death in a rat model of Alzheimer's disease (AD) induced by intracerebroventricular administration of Aβ. We employed the Morris water maze, shuttle box, and open field tests to assess spatial memory, passive avoidance memory, and anxiety-like behavior, respectively. P-Tau and the amyloid precursor protein (APP) expression, along with hippocampal cell death, were also evaluated. Both Aβ and zeolite zinc were injected intracerebroventricularly. The results showed that zeolite zinc partially reversed Aβ-induced impairments in memory performance and mitigated the effects of Aβ on locomotor activity, although it did not fully restore baseline levels. In addition, Aβ increased the expression of APP and P-Tau, as well as the number of dead cells, whereas zeolite zinc reduced these effects. In conclusion, our findings suggest that while zeolite zinc plays a role in modulating the pathophysiology of AD, its therapeutic effects only partially reverse the progression or symptoms of AD, indicating the need for further investigation into optimal dosing or combination therapies.
阿尔茨海默病(AD)是最常见的神经退行性疾病之一,其特征是脑结构和功能缓慢且渐进性丧失,主要影响老年人。有证据表明,大脑中锌稳态的破坏会导致突触功能障碍以及学习和记忆受损。在本研究中,我们评估了沸石锌对脑室注射Aβ诱导的阿尔茨海默病(AD)大鼠模型记忆表现和海马细胞死亡的影响。我们分别采用莫里斯水迷宫、穿梭箱和旷场试验来评估空间记忆、被动回避记忆和焦虑样行为。还评估了P - Tau和淀粉样前体蛋白(APP)的表达以及海马细胞死亡情况。Aβ和沸石锌均通过脑室内注射。结果表明,沸石锌部分逆转了Aβ诱导的记忆表现损伤,并减轻了Aβ对运动活动的影响,尽管它并未完全恢复到基线水平。此外,Aβ增加了APP和P - Tau的表达以及死亡细胞的数量,而沸石锌减轻了这些影响。总之,我们的研究结果表明,虽然沸石锌在调节AD的病理生理学中发挥作用,但其治疗效果仅部分逆转AD的进展或症状,这表明需要进一步研究最佳剂量或联合治疗方法。