Amyloid-beta oligomer (AβO) (AβO)

Amyloid-beta (Aβ) oligomers are soluble, non-fibrillar aggregates of the Aβ peptide that are widely considered the most neurotoxic species in Alzheimer's disease (Selkoe & Hardy, 2016). These oligomers exhibit prion-like properties, meaning they can act as templates to induce the misfolding of healthy Aβ monomers into toxic, self-replicating conformations that spread throughout the brain (Prusiner, 2013; Soto & Pritzkow, 2018). Unlike insoluble amyloid plaques, soluble Aβ oligomers are small enough to diffuse into synaptic clefts where they disrupt synaptic plasticity, impair long-term potentiation, and trigger a cascade of neurodegeneration including tau phosphorylation and neuroinflammation (Walsh & Selkoe, 2007). Modern therapeutic strategies focus on selectively targeting these toxic oligomers and protofibrils to neutralize their seeding activity and facilitate their clearance. Drugs such as lecanemab and the investigational antibody PMN310 are designed to bind these aggregated forms with high affinity while sparing the physiologically necessary Aβ monomers (Eisai, 2023; ProMIS Neurosciences, 2024).

Other names

Toxic Aβ oligomerAmyloid-beta prionSoluble Aβ aggregateAβ seedAβ protofibrilSelf-propagating Amyloid-beta

Monoclonal antibody-mediated clearance of soluble Aβ aggregates, neutralization of toxic oligomer species, and inhibition of prion-like seeding and propagation.