The development of anti–amyloid β–proteins therapy against Alzheimer disease

Abstract

The growing number of people have been suffering from dementia, affecting approximately 45 million individuals worldwide. Alzheimer disease (AD) is a main causative disease of dementia. The accumulation of amyloid β–proteins (Aβ) in the brain is the essential pathogenesis of AD. Based on the Aβ cascade hypothesis, the deposition of the Aβ plaques leads to the tau pathology, neurodegenerative changes, and finally cognitive impairment in AD patients. The development of the different types of anti–Aβ therapy have been attempted, and recently, a huge number of anti–Aβ monoclonal antibodies have been developed. Lecanemab is a representative drug that targets Aβ protofibrils. In this article, we focus on the anti–Aβ therapy and different Aβ species in the aggregation process.