2022 年 39 巻 3 号 p. 379-383
The approval of amyloid β–targeted therapy for Alzheimer disease (AD) in the United States has opened the door for disease–modifying drugs for protinopathies. However, the target of treatment is mild cognitive impairment and/or mild Alzheimer disease (AD), but not advanced AD, and its efficacy is limited. Therefore, there is no doubt about the importance of establishing a therapeutic strategy for tau protein, another pathological indicator of AD. Tau is an accumulation protein that is pathologically correlated with the severity of dementia, and it has been considered as a key molecule that directly leads to neurodegeneration. Therefore, control of tau lesions is the essential therapeutic target in symptomatic AD.
Immunotherapy and nucleic acid therapies are being developed as disease modifying agents for protinopathies. In particular, several clinical trials are underway for tau–targeted antibodies and antisense oligonucleotides. In this article, we will discuss the current status and prospects of disease–modifying drugs against tauopathies.