Several hypotheses have been postulated to explain how Alzheimer’s disease is triggered, but none of them provide a unified view of its pathogenesis. The dominant hypothesis based on build-ups of the amyloid-β peptide has been around for longer than three decades; however, up to today, numerous clinical trials based on the amyloid postulates have been attempted, but all of them have failed. Clearly, the revisited tau hypothesis provides a better explanation of the clinical observations of patients, but it needs to integrate the cumulative observations on the onset of this disease. In this context, the neuroimmuno modulation theory, based on the involvement of inflammatory events in the central nervous system, accounts for all these observations. In this review we intend to emphasize the idea that neuroinflammation is a main target for the search of new therapeutic strategies to control Alzheimer’s disease. Beyond mono-targeting approaches using synthetic drugs that control only specific pathophysiological events, emerging therapeutics views based on multi targeting compounds appear to provide a new pathway for Alzheimer’s disease treatment.

中文翻译：

---

炎症：控制阿尔茨海默氏病的化合物的主要目标

假定了几种假说来解释阿尔茨海默氏病是如何引发的，但没有一个提供有关其发病机理的统一观点。基于淀粉样β肽堆积的主要假设已经存在了超过三十年。然而，直到今天，已经尝试了许多基于淀粉样蛋白假说的临床试验，但是都失败了。显然，重新讨论的tau假说为患者的临床观察提供了更好的解释，但是它需要整合关于这种疾病发作的累积观察。在这种情况下，基于免疫反应参与中枢神经系统的神经免疫调节理论解释了所有这些观察结果。在这篇综述中，我们打算强调以下观点：神经炎症是寻找新的控制阿尔茨海默氏病治疗策略的主要目标。除了使用仅控制特定病理生理事件的合成药物进行单靶点治疗之外，基于多靶点化合物的新兴治疗学观点似乎为阿尔茨海默氏病的治疗提供了新途径。