Department of Chemistry and Nano Science, Ewha Womans University, Seoul 120-750, Korea.
Exp Neurobiol. 2013 Mar;22(1):31-7. doi: 10.5607/en.2013.22.1.31. Epub 2013 Mar 31.
Alzheimer's disease (AD) is a neurodegenerative disease that proceeds with the age-dependent neuronal loss, an irreversible event which causes severe cognitive and psychiatric devastations. In the present study, we investigated whether the compound, AAD-2004 [2-hydroxy-5-[2-(4-trifluoromethylphenyl)-ethylaminobenzoic acid] which has anti-oxidant and anti-inflammatory properties, is beneficial for the brain of Tg-betaCTF99/B6 mice, a murine AD model that was recently developed to display age-dependent neuronal loss and neuritic atrophy in the brain. Administration of AAD-2004 in Tg-betaCTF99/B6 mice from 10 months to 18 months of age completely repressed the accumulation of lipid peroxidation in the brain. AAD-2004 markedly suppressed neuronal loss and neuritic atrophy, and partially reversed depleted expression of calbindin in the brain of Tg-beta-CTF99/B6. These results suggest that AAD-2004 affords neurodegeneration in the brain of AD mouse model.
阿尔茨海默病(AD)是一种神经退行性疾病,随着年龄的增长会出现神经元丧失,这是一种不可逆转的事件,会导致严重的认知和精神损害。在本研究中,我们研究了具有抗氧化和抗炎特性的化合物 AAD-2004[2-羟基-5-[2-(4-三氟甲基苯基)-乙胺基]苯甲酸]是否对 Tg-betaCTF99/B6 小鼠的大脑有益,这是一种最近开发的用于显示大脑中年龄依赖性神经元丧失和神经突萎缩的 AD 模型。从 10 个月到 18 个月大时,在 Tg-betaCTF99/B6 小鼠中给予 AAD-2004 可完全抑制大脑中脂质过氧化的积累。AAD-2004 显著抑制神经元丧失和神经突萎缩,并部分逆转 Tg-beta-CTF99/B6 小鼠大脑中钙结合蛋白的耗竭表达。这些结果表明,AAD-2004 可防止 AD 小鼠模型的神经退行性变。