Researchers have described, for the first time, the structure of a type of amyloid beta plaque protein linked to Alzheimer’s disease (AD) progression. The study found that small aggregates of the amyloid beta protein can float through the brain tissue fluid, reaching multiple areas of the brain and disrupting local neuron functioning. The research also provided evidence that a newly approved AD treatment, lecanemab, could neutralize these small, diffusible aggregates. A phase III clinical trial found that lecanemab slowed cognitive decline in patients with early AD, with its positive effect potentially being linked to its ability to bind and neutralize soluble amyloid beta protein aggregates, or oligomers. The researchers isolated the free-floating aggregates by soaking postmortem brain tissues from typical AD patients in saline solutions and determined the atomic structure of these tiny aggregates, down to the individual atom. The team plans to observe how the tiny amyloid beta aggregates travel through living animal brains and study how the immune system responds to these toxic substances.