Alzheimer's disease (AD) was first described by Alois Alzheimer in 1906 but the protein composition of neurofibrillary tangles and amyloid plaques was not decoded till about seven to eight decades later, respectively. The bulk of studies during the last four decades were focused on Aβ amyloid and led to many human clinical trials, none of which showed any beneficial therapeutic effects. Though the outcome of prodromal Aβ immunotherapy in carriers of AD-causing gene mutations is still awaited, this has led to a shift away from Aβ-based, toward tau-based, therapeutic approaches. Currently, several Phase I and Phase II human clinical trials are underway, the majority of which involve active or passive tau immunization. It is quite possible that along with inhibition of tau pathology, use of neurotrophic compounds that can enhance neurogenesis and neuronal plasticity will be required to effectively prevent and restore cognitive deficits in AD and related conditions. Investments need to be made in drug development of such compounds.

Alois Alzheimer于1906年首次描述了阿尔茨海默氏病（AD），但直到大约七到八十年后，神经原纤维缠结和淀粉样蛋白斑的蛋白质组成才被解码。在过去的40年中，大部分研究都集中在Aβ淀粉样蛋白上，并导致了许​​多人类临床试验，但都没有显示出任何有益的治疗作用。尽管仍在等待引起AD基因突变的携带者进行前驱性Aβ免疫治疗的结果，但这已导致从基于Aβ的治疗方法转向基于tau的治疗方法。当前，一些I期和II期人类临床试验正在进行中，其中大多数涉及主动或被动tau免疫。很有可能伴随着tau病理学的抑制，需要使用能够增强神经发生和神经元可塑性的神经营养化合物来有效预防和恢复AD及相关疾病的认知缺陷。需要在这类化合物的药物开发中进行投资。