Thorajak Piyaporn, Pannangrong Wanassanun, Welbat Jariya Umka, Chaijaroonkhanarak Wunnee, Sripanidkulchai Kittisak, Sripanidkulchai Bungorn
Department of Anatomy, Faculty of Medicine, Khon Kaen University, Khon Kaen 40002, Thailand.
Center for Research and Development of Herbal Health Products, Khon Kaen University, Khon Kaen 40002, Thailand.
Nutrients. 2017 Jul 1;9(7):686. doi: 10.3390/nu9070686.
Alzheimer's disease (AD) has been linked to the degeneration of central cholinergic and glutamatergic transmission, which correlates with progressive memory loss and the accumulation of amyloid-β (Aβ). It has been claimed that aged garlic extract (AGE) has a beneficial effect in preventing neurodegeneration in AD. Therefore, the objective of this study was to investigate the effects of AGE on Aβ-induced cognitive dysfunction with a biochemical basis in the cholinergic, glutamatergic, and GABAergic systems in rats. Adult male Wistar rats were orally administered three doses of AGE (125, 250, and 500 mg/kg) daily for 65 days. At day 56, they were injected with 1 μL of aggregated Aβ (1-42) into each lateral ventricle, bilaterally. After six days of Aβ injection, the rats' working and reference memory was tested using a radial arm maze. The rats were then euthanized to investigate any changes to the cholinergic neurons, vesicular glutamate transporter 1 and 2 proteins (VGLUT1 and VGLUT2), and glutamate decarboxylase (GAD) in the hippocampus. The results showed that AGE significantly improved the working memory and tended to improve the reference memory in cognitively-impaired rats. In addition, AGE significantly ameliorated the loss of cholinergic neurons and increased the VGLUT1 and GAD levels in the hippocampus of rat brains with Aβ-induced toxicity. In contrast, the VGLUT2 protein levels did not change in any of the treated groups. We concluded that AGE was able to attenuate the impairment of working memory via the modification of cholinergic neurons, VGLUT1, and GAD in the hippocampus of Aβ-induced rats.
阿尔茨海默病（AD）与中枢胆碱能和谷氨酸能传递的退化有关，这与进行性记忆丧失和β-淀粉样蛋白（Aβ）的积累相关。据称， aged garlic extract（AGE）在预防AD中的神经退行性变方面具有有益作用。因此，本研究的目的是在大鼠的胆碱能、谷氨酸能和γ-氨基丁酸能系统中，研究AGE对Aβ诱导的认知功能障碍的影响及其生化基础。成年雄性Wistar大鼠每天口服三剂AGE（125、250和500mg/kg），持续65天。在第56天，双侧向每个侧脑室内注射1μL聚集的Aβ（1-42）。注射Aβ六天后，使用放射状臂迷宫测试大鼠的工作记忆和参考记忆。然后对大鼠实施安乐死，以研究海马体中胆碱能神经元、囊泡谷氨酸转运体1和2蛋白（VGLUT1和VGLUT2）以及谷氨酸脱羧酶（GAD）的任何变化。结果表明，AGE显著改善了认知受损大鼠的工作记忆，并倾向于改善其参考记忆。此外，AGE显著改善了胆碱能神经元的丧失，并提高了Aβ诱导毒性的大鼠脑海马体中VGLUT1和GAD的水平。相比之下，在任何治疗组中，VGLUT2蛋白水平均未发生变化。我们得出结论，AGE能够通过改变Aβ诱导大鼠海马体中的胆碱能神经元、VGLUT1和GAD来减轻工作记忆的损害。
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