Lecanemab: A Targeted Approach to Beta Amyloid Reduction in Alzheimer’s Disease

Abstract

Alzheimer's disease is a progressive neurological disorder that primarily affects older adults and is the most common cause of dementia. It involves the degeneration of brain cells, leading to memory loss, cognitive decline, and changes in behavior and personality. Worldwide, an estimated 50 million people are living with dementia, and Alzheimer's disease accounts for approximately 60-70% of these cases and by 2050 the number of people with Alzheimer's is expected to triple, reaching about 150 million globally, primarily due to the aging population. Currently available treatments only halts the symptoms of the disease, and the underlying pathology remains untouched; thus, there is progressive deterioration due to the intact pathology. Various drugs are being researched to address the complex neuropathology of AD. The FDA's approval of lecanemab marks a significant advancement in Alzheimer's disease treatment, as it targets the underlying pathology of the disease rather than just alleviating symptoms. This shift in focus from symptomatic treatments to addressing the root cause is exemplified by lecanemab's ability to reduce amyloid-beta (Aβ) plaques, and its clinical properties highlight its potential for improving patient outcomes. This paper provides a thorough review of the efficacy and safety of lecanemab, a monoclonal antibody, with an emphasis on its binding properties and clinical trial data. Lecanemab stands out from other monoclonal antibodies due to its remarkable affinity for hazardous Aβ protofibrils. Clinical trials have yielded promising outcomes, including lower amyloid load, improved cognitive assessments, and a slower rate of cognitive decline. This review article aims to provide a comprehensive overview of Alzheimer’s disease, focusing on its epidemiology, risk factors, pathophysiology, and the emerging role of lecanemab as a potential disease-modifying therapy. By comparing lecanemab with existing symptomatic treatments that primarily address symptoms rather than underlying pathology, this review emphasizes the importance of targeting the fundamental mechanisms of AD for improved patient outcomes. Furthermore, it underscores the necessity for continued research to refine treatment strategies and enhance our understanding of this complex disease to better serve affected individuals and their families.