William E. Van Nostrand

TL;DR: It is shown that low-temperature and low-salt conditions can stabilize disc-shaped oligomers (pentamers) that are substantially more toxic to mouse cortical neurons than protofibrils and fibrils, and that these neurotoxic oligomers do not have the β-sheet structure characteristic of fibril.

TL;DR: Low-affinity LRP/Aβ interaction and/or Aβ-induced LRP loss at the BBB mediate brain accumulation of neurotoxic Aβ in transgenic mice and patients with cerebrovascular β-amyloidosis.

TL;DR: The findings confirmed that treatment of microglia with anti-inflammatory cytokines such as IL-4 and IL-13 induces a gene profile typical of alternative activation similar to that previously observed in peripheral macrophages and suggest that innate immune cells in AD may exhibit a hybrid activation state that includes characteristics of classical and alternative activation.

TL;DR: It is shown that overexpression of human AβPP is not required for early-onset and robust accumulation of both vascular and parenchymal Aβ in mouse brain, and in vivo transport studies demonstrated that Dutch/Iowa mutant Aβ was more readily retained in the brain compared with wild-type Aβ.

TL;DR: Whereas the A21G Flemish mutation appears to enhance Aβ production, the E22Q Dutch and D23N Iowa mutations enhance fibrillogenesis and the pathogenicity of Aβ toward HCSM cells, suggesting that the different CAA mutations in AβPP may exert their pathogenic effects through different mechanisms.