Raskatov argues P3, once judged harmless, deserves study beside amyloid beta in Alzheimer's

Raskatov hedges his own claim in the same breath as he makes it. "The P3 peptide is, most likely, not the innocent bystander it was commonly thought to be. There's still more research to be done. But this could turn Alzheimer's research on its head," he said ^[11]. We would weight the first two sentences of that quote above the third.

The document is a commentary ^[1]. The speed comparison with amyloid beta appears in the university's summary of it ^[2]. The summary does not say which assays produced the comparison, at what concentrations, or whether P3 aggregates have been found in patient brain tissue. The thing this doesn't tell you is how much P3 sits beside amyloid beta in a living brain.

Raskatov's laboratory studies amyloid peptides ^[12], so he is arguing for a relative of his own subject. His case rests on the field's record. Antibodies such as lecanemab and donanemab are approved to help remove amyloid beta ^[6], and he argues the benefits so far remain limited ^[7]. Some treatments have also been associated with brain hemorrhages and strokes ^[5]. "Progress has been extremely slow, and the current state of the art in Alzheimer's therapy leaves much to be desired," he said ^[8].

In our view the interaction claim is the one to test first. A P3 that only clumps on its own adds a second target to study. A P3 that changes how toxic amyloid beta becomes would also bear on how results from amyloid-directed treatments are read.