Monoclonal Antibody Therapy in Early Alzheimer’s disease: a Review of Lecanemab and Aducanumab
Keywords:
Alzheimer's disease, Lecanemab, Aducanumab, Anti-Amyloid monoclonal antibodies, β-amyloid protofibrilsAbstract
Alzheimer's disease (AD) is a tragic and progressive neurodegenerative condition that impinges on the quality of life of the patient and impacting millions of people globally. Lecanemab (Leqembi) and Aducanumab (Aduhelm) are monoclonal antibody therapies for early Alzheimer's disease that bind and clear beta-amyloid plaques from the brain. Lecanemab targets β-amyloid protofibrils, has demonstrated encouraging efficacy in Phase III clinical trials for the therapy of early Alzheimer's disease (AD). Lecanemab has been approved by the FDA and has demonstrated significant efficacy in lowering Aβ plaque, thus treating the pathology. The therapy is given every two weeks via IV, taking approximately one hour to perform for each infusion. Magnetic resonance imaging (MRI) scans prior to initiation of treatment with lecanemab. Individuals have a genetic risk factor (ApoE ε4 gene carriers) that can result in an increased risk for the side effect of amyloid- related imaging abnormalities (ARIA). Lecanemab and Aducanumab can lead to amyloid-related imaging abnormalities (ARIA). ARIA is usually asymptomatic, but life-threatening and dangerous events are uncommon. ARIA leads to transient cerebral swelling that can be resolved with time and can be associated with bleeding in minor regions of the brain, but some individuals might present with symptoms like headache, confusion, dizziness, and changes in vision, nausea, and seizure. Aducanumab targets aggregated forms (plaque) of amyloid beta (Aβ) found in the brains of people with Alzheimer's disease to reduce its buildup. USFDA approved aducanumab onJuly, 2021, under accelerated approval, the first and sole treatment that addresses a major pathology of AD through the reduction of Aβ plaques in the brain.
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