Research on AD, or Alzheimer's disease, influenced via amyloid theory. But our knowledge of this framework has changed dramatically as a result of mounting clinical, genetic, and molecular evidence. It is now widely acknowledged that the most dangerous forms of Aβ are the smaller, soluble oligomers, early protofibrils, and quickly forming aggregates produced by processes like secondary nucleation and supersaturation, rather than the large, mature fibrils that were previously believed to be central to the disease. Amyloid toxicity is highly dependent on individual biological context, as seen by the significant influence of genetic variables, particularly APOE ε4 and TREM2 variations, on how the brain clears Aβ, how microglia react, and how well proteostasis is maintained. In this review, we give a summary of all available treatment approaches targeted at decreasing the generation of Aβ, preventing its aggregation, and improving its elimination. The clinical advantages, side-effect profiles, and practical issues, such as the requirement for close monitoring of ARIA, of the newly licensed anti-amyloid antibodies aducanumab, lecanemab, and donanemab are analyzed.
Lawate* et al. (2026) studied this question.