Amyloid-beta (Aβ) and Tau proteins (Aβ and Tau)

Amyloid-beta (Aβ) and Tau proteins are the primary pathological hallmarks of Alzheimer's disease (AD) and related neurodegenerative disorders known as tauopathies. Amyloid-beta, particularly the Aβ1-40 and Aβ1-42 isoforms, is generated by the proteolytic cleavage of the amyloid precursor protein (APP) and aggregates into extracellular plaques that disrupt synaptic communication and trigger neuroinflammation [1, 2]. Tau is a microtubule-associated protein that normally stabilizes axons, but in disease, it undergoes hyperphosphorylation, leading to the formation of intracellular neurofibrillary tangles (NFTs) that cause neuronal death [3]. The amyloid cascade hypothesis posits that Aβ accumulation is the initiating event in AD, which subsequently drives tau pathology and cognitive decline [4]. Therapeutic interventions primarily focus on monoclonal antibodies, such as lecanemab and donanemab, which target and clear Aβ aggregates from the brain [5]. Emerging tau-targeted therapies aim to prevent the spread of toxic tau species or inhibit the kinases responsible for its pathological phosphorylation [6].

Other names

AbetaAβ42Aβ40MAPTMicrotubule-associated protein tauNeurofibrillary tanglesAmyloid plaquesTau

Monoclonal antibody-mediated clearance of protein aggregates; inhibition of protein aggregation; modulation of secretase activity; inhibition of tau phosphorylation.