Cacao Ameliorates Amyloid Beta-Induced Cognitive and Non-Cognitive Disturbances.

IF 2.9 Q2 NEUROSCIENCES
Neuroscience Insights Pub Date : 2024-09-17 eCollection Date: 2024-01-01 DOI:10.1177/26331055241280638
Hamid Shokati Basir, Naser Mirazi, Alireza Komaki, Mahdi Ramezani, Abdolkarim Hosseini
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Abstract

Background: Alzheimer's disease (AD) is a progressive neurological disorder characterized by a wide range of cognitive and non-cognitive impairments. The present study was designed to investigate the potential effects of cacao on cognitive and non-cognitive performance and to identify the role of oxidative stress in an AD animal model induced by unilateral intracerebroventricular (U-ICV) injection of amyloid beta1-42 (Aβ1-42).

Methods: Oral administration of cacao (0.5 g/kg/day) was performed for 60 consecutive days. Following 60 days, the open-field (OF) test, elevated plus-maze (EPM) test, novel object recognition (NOR) test, Barnes maze (BM) test, and Morris water maze (MWM) test were used to evaluate locomotor activity, anxiety-like behavior, recognition memory, and spatial memory, respectively. Total oxidant status (TOS) and total antioxidant capacity (TAC) in plasma were also examined. Furthermore, the number of healthy cells in the hippocampus's dentate gyrus (DG), CA1, and CA3 regions were identified using hematoxylin and eosin staining.

Results: The results indicated that the injection of Aβ1-42 in rats led to recognition memory and spatial memory impairments, as well as increased anxiety. This was accompanied by decreased total antioxidant capacity (TAC), increased total oxidative stress (TOS), and increased neuronal death. Conversely, cacao treatment in AD rats improved memory function, reduced anxiety, modulated oxidative stress balance, and decreased neuronal death.

Conclusion: The findings suggest that cacao's ability to improve the balance between oxidants and antioxidants and prevent neuronal loss may be the mechanism underlying its beneficial effect against AD-related cognitive and non-cognitive impairments.

可可能改善淀粉样β蛋白诱发的认知和非认知紊乱
背景:阿尔茨海默病(AD)是一种进行性神经系统疾病,其特征是广泛的认知和非认知功能障碍。本研究旨在探讨可可对认知和非认知能力的潜在影响,并确定氧化应激在单侧脑室内注射淀粉样β1-42(Aβ1-42)诱导的阿尔茨海默病动物模型中的作用:方法:连续60天口服可可(0.5克/千克/天)。60天后,分别使用开阔地(OF)测试、高架迷宫(EPM)测试、新物体识别(NOR)测试、巴恩斯迷宫(BM)测试和莫里斯水迷宫(MWM)测试来评估运动活性、焦虑样行为、识别记忆和空间记忆。此外,还检测了血浆中的总氧化状态(TOS)和总抗氧化能力(TAC)。此外,还使用苏木精和伊红染色法鉴定了海马齿状回(DG)、CA1和CA3区健康细胞的数量:结果表明,给大鼠注射 Aβ1-42 会导致识别记忆和空间记忆受损,并增加焦虑。与此同时,总抗氧化能力(TAC)下降,总氧化应激(TOS)增加,神经元死亡增加。与此相反,对AD大鼠进行可可治疗可改善其记忆功能,减轻焦虑,调节氧化应激平衡,减少神经元死亡:结论:研究结果表明,可可能够改善氧化剂和抗氧化剂之间的平衡,防止神经元损失,这可能是可可对与阿德相关的认知和非认知障碍产生有益影响的机制。
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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来源期刊
Neuroscience Insights
Neuroscience Insights Neuroscience-Neuroscience (all)
CiteScore
6.10
自引率
0.00%
发文量
24
审稿时长
9 weeks
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