Alzheimer's disease (AD) is a chronic and progressive neurodegenerative disorder characterized by abnormal accumulation of extracellular β-amyloid (Aβ) plaques and neuronal damage. The present study investigated the effect of chronic intra-hippocampal agmatine administration on β-Amyloid (Aβ) induced memory impairment in mice. Aβ_1-42 peptide injected mice demonstrated impairment of cognitive abilities evaluated as reference memory error and working memory error in radial arm maze (RAM) and decreased exploration time for novel object as well as recognition index in novel object recognition (NOR) test along with elevation in Aβ_1-42 peptide, β-Site APP cleaving enzyme 1 (BACE 1), microtubule-associated protein tau (MAPt), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and reduction in neprilysin and brain derived neurotrophic factor (BDNF) immunocontent within hippocampus and prefrontal cortex. Importantly, this was associated with a reduction in the agmatine levels following Aβ_1-42 peptide administration. Chronic administration of agmatine from day 8–27, prevented the memory impairment in mice and normalized the neurochemical alteration within prefrontal cortex and hippocampus induced by Aβ_1-42 peptide administration. However, it did not modulate the amyloid precursor protein and BACE expression. This study suggests that agmatine improves learning and memory impairment possibly through the down regulation of neuroinflammatory pathways in AD.

阿尔茨海默氏病（AD）是一种慢性进行性神经退行性疾病，其特征在于细胞外β-淀粉样蛋白（Aβ）斑块异常积聚和神经元损伤。本研究调查了慢性海马内胍丁胺给药对β-淀粉样蛋白（Aβ）诱导的小鼠记忆障碍的影响。Aβ _1-42肽注射的小鼠表现出评价为在放射臂迷宫（RAM）参考存储器错误和工作记忆错误认知能力的损害和降低勘探时间为新物体，以及在伴随着新物体识别（NOR）试验识别指数_{Aβ1-42处的}海拔肽，β-位点APP裂解酶1（BACE 1），微管相关蛋白tau（MAPt），白介素6（IL-6），肿瘤坏死因子-α（TNF-α）以及脑啡肽酶和脑源性神经营养减少海马和额叶前额叶皮层内的BDNF（BDNF）免疫含量。重要的是，这与施用_Aβ1-42肽后胍丁胺水平的降低有关。从第8–27天开始长期服用胍丁胺，可以预防小鼠的记忆障碍，并使_Aβ1-42诱导的额叶皮层和海马神经化学改变正常化肽给药。但是，它不能调节淀粉样蛋白前体蛋白和BACE表达。这项研究表明，胍丁胺可能通过下调AD中的神经炎症途径来改善学习和记忆障碍。