Abstract: Alzheimer’s disease (AD) is the most prevalent form of dementia, i.e., progressive memory loss and profound cognitive dysfunction, resulting in a considerable societal burden. At the neuropathological level, the brains of AD patients exhibit amyloid-β (Aβ) plaques, neurofibrillary tangles, and neuroinflammation (Sala Frigerio and De Strooper, 2016). The growing number of individuals affected with AD underscores the pressing need for the development of effective treatments, and a cure remains elusive. The pathogenesis of AD involves intricate molecular and cellular mechanisms that lead to progressive neurodegeneration and cognitive decline. A central tenet of AD pathogenesis is the amyloid cascade hypothesis, which posits that the accumulation of Aβ peptides plays a pivotal role in disease progression. Aβ derives from the amyloid precursor protein (APP) by BACE1 (β-secretase) and γ-secretase cleavages, and aggregates into plaques that eventually disrupt neuronal function. Concurrently, abnormal phosphorylation of the tau protein leads to the formation of neurofibrillary tangles, contributing to neuronal degeneration. Neuroinflammation, oxidative stress, mitochondrial dysfunction, and synaptic impairment further compound the pathology (Sala Frigerio and De Strooper, 2016). The intricate interplay of these phenomena underscores the challenges in treating AD, necessitating innovative therapeutic approaches to halt or slow disease progression effectively. Recently, monoclonal antibody drugs, like Aducanumab, Lecanemab, and Donanemab, have shown the ability to decelerate memory and cognitive decline in phase III clinical trials of early-stage AD (Boxer and Sperling, 2023). Aducanumab is designed to bind Aβ aggregates in both the oligomeric and fibrillar states rather than amyloid monomers, while Lecanemab has been proposed to target so called Aβ protofibrils. Donanemab is directed against N-terminally modified form of Aβ. These clinical trials collectively suggest that the approach to target Aβ represents an effective strategy for treating AD, particularly in its early stages.