Amyloid-beta plaque (Aβ plaque) (Aβ plaque)

Fibrillar amyloid-beta (Aβ) plaques are extracellular protein aggregates primarily composed of Aβ42 peptides, which are proteolytic cleavage products of the amyloid precursor protein (APP) [1, 14]. These plaques are a hallmark pathological feature of Alzheimer's disease and are found in the brain's gray matter, where they disrupt synaptic function and trigger neurotoxic cascades, including oxidative stress and neuroinflammation [17, 19, 20]. In the context of drug development, these plaques serve as a primary therapeutic target for disease-modifying treatments, particularly monoclonal antibodies [5, 16]. These antibodies, such as lecanemab and donanemab, are designed to bind to the aggregated Aβ species, facilitating their clearance by the brain's immune cells, such as microglia [5, 9]. While successful plaque reduction has been linked to a slowing of cognitive decline in early-stage Alzheimer's patients, the treatment is associated with significant safety concerns, most notably amyloid-related imaging abnormalities (ARIA) [7, 8, 10].

Other names

Senile plaqueNeuritic plaqueAmyloid plaqueExtracellular amyloid-beta depositAβ fibril

Passive immunotherapy using monoclonal antibodies that bind to fibrillar amyloid-beta aggregates, facilitating their clearance through microglial-mediated phagocytosis and plaque dissolution [5, 9, 12].