Science
Leveraging our deep understanding of amyloid-beta oligomers to usher in a medical breakthrough for Alzheimer’s disease.
AMYLOID-BETA OLIGOMERS (AβOs)
In Alzheimer’s patients, three dominant pools of amyloid-beta (Aβ) species have been identified: Aβ monomers, Aβ oligomers (AβOs) and fibrillar Aβ aggregates that deposit into amyloid plaques. The most abundant species, Aβ monomers, as well as Aβ plaques, have been the main focus of Alzheimer’s drug development efforts throughout the past decade.
However, at Acumen, our team is focused solely on the less prevalent AβOs. These soluble protein aggregates disrupt brain circuitry and prevent neurons from functioning properly. The accumulation of AβOs is associated with synapse deterioration and loss, tau phosphorylation and inflammation. Overwhelming scientific evidence now indicates AβOs are the most toxic form of amyloid, leading to the memory and cognitive impairment and chronic neurodegeneration now known as the hallmark of Alzheimer’s disease.
Recent laboratory studies suggest eliminating these toxic soluble AβOs from the system may even enable these damaged circuits to regain some of their function. We are developing ACU193, an anti-AβO monoclonal antibody with best-in-class potential for superior efficacy and safety in Alzheimer’s disease.
Recent laboratory studies suggest eliminating these amyloid-beta oligomers from the system may even enable these damaged circuits to regain some of their function. We are developing ACU193, an anti-AβOs monoclonal antibody with best-in-class potential for efficacy and safety in Alzheimer’s disease.
