Cognitive Neurology Unit, Department of Neurology, Hospital del Salvador & Department of Geriatrics, Clinical Hospital, University of Chile, Chile.
Curr Alzheimer Res. 2011 Sep;8(6):686-8. doi: 10.2174/156720511796717221.
Alzheimer΄s Disease (AD) physiopathology is not yet totally established. Nevertheless it is known that a metabolism dysfunction of the amyloid beta precursor protein (APP) and the abnormal tau protein phosphorylation lead to the formation of neuritic plaques and neurofibrillary tangles, respectively. These events finally drive to the clinical expression of dementia. Formally approved during the past decade, treatments for AD are lacking of an updating, being essentially symptomatic. Anticholinesterase agents have failed in providing a substantial improvement in the mental health condition of AD patients. On the other hand, antiamyloid strategies, have failed in their efficacy or security on their last development phases. In this context, tau represents a potential therapeutic target, by the action of drugs that diminish its aggregation, or acting by altering its phosphorylation or filaments formation. There is also anti-tau miscellaneous strategies such as normal microtubule-stabilizing agents. Thus, it might be possible that in a near future the neurodegenerative process could be stopped.
阿尔茨海默病（AD）的发病机制尚未完全确定。然而，已知淀粉样前体蛋白（APP）的代谢功能障碍和异常的 tau 蛋白磷酸化分别导致神经原纤维缠结和神经纤维缠结的形成。这些事件最终导致痴呆的临床表达。在过去十年中正式批准的 AD 治疗方法缺乏更新，主要是对症治疗。胆碱酯酶抑制剂未能显著改善 AD 患者的心理健康状况。另一方面，抗淀粉样蛋白策略在其最后开发阶段的疗效或安全性方面都失败了。在这种情况下，tau 代表了一个潜在的治疗靶点，通过减少其聚集的药物的作用，或通过改变其磷酸化或丝形成来发挥作用。还有其他的抗 tau 策略，如正常的微管稳定剂。因此，在不久的将来，神经退行性过程可能会停止。
