Interpretive article from ALZFORUM:
[The research] debut a small molecule, DAPPD, that seems to fit the bill. DAPPD resembles acetaminophen and enters the brain easily. In two mouse models of amyloidosis, chronic administration lightened amyloid load and preserved memory. Studies with cultured mouse and human cells found that DAPDD acts specifically on microglia, blocking the activation of the NLRP3 inflammasome. This lowered inflammatory signaling and stimulated phagocytosis.
The [paywalled] paper was:
Park MH, Lee M, Nam G, Kim M, Kang J, Choi BJ, Jeong MS, Park KH, Han WH, Tak E, Kim MS, Lee J, Lin Y, Lee YH, Song IS, Choi MK, Lee JY, Jin HK, Bae JS, Lim MH.
N,N'-Diacetyl-p-phenylenediamine restores microglial phagocytosis and improves cognitive defects in Alzheimer's disease transgenic mice.
Proc Natl Acad Sci U S A. 2019 Nov 4; PubMed.
I found this more interesting because I took a short "personal enrichment" type class on the NLRP3 inflammasome a couple of months ago, although the post-doc teaching it was more focused on the interaction of NLRP3 and the inflammatory response in macrophages, rather than microglia and macro phenomena like AD.