/         阿尔茨海默病(AD)是一种慢性神经退行性疾病，主要表现为进行性记忆丧失。基因突变产生淀粉样蛋白β (Aβ)，是淀粉样蛋白β (Aβ)早期变异症状，目前广泛认为淀粉样蛋白β (Aβ)是被认为是环境因素和各种基因之间的相互作用的结果。近期在这方面取得了突破，12 / 15脂氧合酶(12/15LO)通路可能在阿尔茨海默病(AD)的发病机制中发挥重要作用。2015年3月发表于《Trends in pharmacological sciences》(药理学趋势)杂志的一篇文章介绍了相关内容。

        文章指出12 / 15LO广泛分布在中枢神经系统，其表达水平与在阿尔茨海默病(AD)或轻度认知功能障碍患者中升高达。研究者利用动物模型对12/15LO在阿尔茨海默病(AD)中的分子病理机制进行研究。研究指标包括淀粉样蛋白β (Aβ)、tau蛋白的代谢、突触的完整性和认知功能等。文章介绍了这种途径与AD发病机制的相关性，讨论其中的机制，并介绍了如何靶向12 / 15LO，来发展新的AD治疗药物。

        Trends Pharmacol Sci. 2015 Mar;36(3):181-6. doi: 10.1016/j.tips.2015.01.005. Epub 2015 Feb 20.

        The 12/15-lipoxygenase as an emerging therapeutic target for Alzheimer's disease.

        Joshi YB1, Giannopoulos PF1, Praticò D2.

        Author information

        Abstract

        Alzheimer's disease (AD) is a chronic neurodegenerative condition characterized by progressive memory loss. Mutations in genes involved in the production of amyloid-β (Aβ) are linked to the early-onset variant of AD. However, the most common form, sporadic AD, is considered to be the result of an interaction between environmental risk factors and various genes. Among them, recent work has highlighted the potential role that the 12/15-lipoxygenase (12/15LO) pathway may play in AD pathogenesis. 12/15LO is widely distributed in the central nervous system, and its levels are upregulated in patients with AD or mild cognitive impairments. Studies using animal models have implicated 12/15LO in the molecular pathology of AD, including the metabolism of Aβ and tau, synaptic integrity, and cognitive functions. We provide an overview of this pathway and its relevance to AD pathogenesis, discuss the mechanism(s) involved, and provide an assessment of how targeting 12/15LO could lead to novel AD therapeutics.