Overview

• Scientists report that midkine prevents amyloid‑beta from sticking together and lowers its accumulation in Alzheimer’s disease models.
• Kinetic modeling of thioflavin T fluorescence data indicates blocked elongation and secondary nucleation, a result corroborated by NMR.
• Complementary biophysical techniques, including circular dichroism and electron microscopy, characterized the disruption of fibril formation.
• Genetic deletion of the midkine gene in Alzheimer’s mouse models increased amyloid‑beta assemblies, supporting a protective role in vivo.
• Research teams from St. Jude and Van Andel, backed by NIH and other funders, now aim to map the binding interface to enable small‑molecule development.