UCLA

Alzheimer's disease is a devastating disorder that is estimated to affect more than 25 million people worldwide and for which there are no preventive, disease-modifying, or curative therapies. Substantial evidence indicates that the amyloid β-protein (Aβ) is a seminal factor in disease causation and may be a tractable therapeutic target. The ability of Aβ to self-associate to form oligomeric assemblies appears to underlie the early toxic events that lead to memory impairment and subsequent neurodegeneration. We review here research on Aβ folding, self-assembly, and toxicity, highlighting areas critical for the development of efficacious Aβ-directed therapeutics.