“…Cells were grown to confluence. On the day of treatment, media was replaced with fresh media containing either no inhibitor or one or more of the following inhibitors: insulin (100 μM), a competitive inhibitor of IDE (Edland, 2004); phenylmethylsulphonyl fluoride (PMSF, 0.5 mM), an inhibitor of serine proteases (Barr and Warner, 2003); 1,10 phenanthroline (2 mM), a non‐competitive inhibitor of IDE (Harada et al, 1993); ethylenediamine tetraacetic acid (EDTA, 5mM), a chelator of divalent ions (Kim et al, 2005); 5,5′‐dithiobis (2‐nitrobenzoic acid) (DTNB, 2 mM), a membrane impermeable modifier of thiol groups (Zoccarato et al, 1999); thiorphan (100 nM), a specific neprilysin inhibitor (Roques et al, 1980); phosphoramidon (1 μM), a specific inhibitor of endothelin converting enzyme (Ikegawa et al, 1990); phenylarsine oxide (PAO, 20 μM), an endocytosis inhibitor (Foley et al, 2005); sucrose (0.5 mM), an endocytosis inhibitor (Nieland et al, 2005); or filipin complex IV (Fil, 10 μg/ml), an inhibitor of caveolae mediated endocytosis (Schnitzer et al, 1994). At the time of treatment cells were brought to 10–20 pM with [ 125 I] Aβ 1–40 and samples were taken at the times specified.…”