Abstract
Visualization of amyloid fibrils by in-vivo imaging techniques accordingly offers diagnostic information at a prodromal stage of the disease, and facilitates therapeutic evaluations during the course of emerging anti-amyloid treatments. By comparing findings in positron emission tomographic (PET) amyloid imaging of AD and model mouse brains, an N-terminally cleaved and modified Aβ termed AβN3 (pE) has been identified as a major constituent of “AD-like” Aβ plaques enriched with binding sites for imaging agents. Clarification of the molecular pathogenesis and development of diagnostic and therapeutic agents can synergistically promote each other with the aid of molecular imaging technologies. Other elements such as tau inclusions and activated microglia in living brains would be of vital significance.
