Unraveling Alzheimer’s: the promise of aducanumab, lecanemab, and donanemab

Abstract

Abstract Alzheimer’s disease (AD) is a neurodegenerative condition that causes cognitive decline, memory loss, and reduced personal autonomy. The pathology of AD involves the aggregation of abnormal brain proteins, specifically beta-amyloid plaques and tau tangles, disrupting neuronal communication and leading to the loss of brain cells. Aducanumab, a monoclonal antibody, demonstrates promise in clinical trials by selectively binding to aggregated amyloid-beta, leading to a notable decrease in plaque burden and potential cognitive benefits. However, regulatory approval for aducanumab remains controversial. Lecanemab and donanemab are recent additions to the AD’s treatment landscape, both targeting aggregated amyloid-beta. Lecanemab shares similarities with aducanumab in its mechanism of action, while donanemab employs a distinct approach by binding to a specific truncated form of amyloid-beta. Positive outcomes have been observed in early-stage clinical trials for both drugs, demonstrating a reduction in amyloid-beta plaques. While aducanumab’s approval offers hope for AD’s treatment, ongoing studies on lecanemab and donanemab are imperative for a comprehensive understanding of their potential in disease modification. Here, we show in this review the potential AD treatments, with a focus on their primary action targeting the reduction of amyloid-beta plaques ultimately giving a broader insight on the topic. The review emphasizes the necessity for long-term efficacy and safety data to assess the overall impact of these drugs on cognitive decline and functional outcomes for future researchers to endeavor. In conclusion, the development of amyloid-beta targeting monoclonal antibodies represents a significant stride in AD’s treatment, demanding further investigation to ascertain their true potential and role in the therapeutic arsenal for this challenging condition.

Keywords

• Alzheimer disease
• Tau proteins
• Aducanumab
• Antibodies
• Monoclonal
• Humanized