The abnormal accumulation and aggregation of amyloid β (Aβ) is one of the key factors of the synaptic impairment in Alzheimer's disease. Biomolecules, e.g., apolipoproteins, and membrane receptors, are implicated in the aggregation and toxicity of Aβ. Engineered molecules, such as enzymes, antibodies, and nanoparticles, are designed to interfere with these processes. We compile structural information on these molecules and their essential roles in the complex processes of aggregation, disaggregation, degradation, clearance, and inhibition of Aβ. The interactions between Aβ and its partners have no obvious emerging commonalities. One exception is the recognition of the N-terminal region of Aβ peptides by antibody heavy and light chains, which are facilitated by cooperative interaction not observed in other Aβ-peptide molecules. Overall, the emerging picture charts a diverse, to date unexplored, landscape and serves as the first-of-its-kind partner- and scenario-specific analysis.
- Alzheimer's disease therapies
- amyloid beta-peptides
- amyloid β-interacting partners
- monoclonal antibody