Aβ peptide vaccination prevents memory loss in an animal model of Alzheimer's disease

By D. Morgan, D. Diamond, P. Gottschall, K. Ugen, C. Dickey, John Hardy, K. Duff, P. Jantzen, G. Dicarlo, D. Wilcock and 5 more. Nature, 2000

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Curcumin has potent anti‐amyloidogenic effects for Alzheimer's β‐amyloid fibrils in vitro (2004, background): “Vaccination (Schenk et al., 1999; Janus et al., 2000; Morgan et al., 2000) and secretase inhibitors (Skovronsky et al., 2000) have been reported as experimental therapies and for clinical trials.”
Soluble Aβ oligomers inhibit long-term potentiation through a mechanism involving excessive activation of extrasynaptic NR2B-containing NMDA receptors (2011, background): “Importantly, A immunotherapy can protect against the neuropathology and cognitive deficits observed in APP transgenic mice (Janus et al., 2000; Morgan et al., 2000) and also prevent the LTP inhibition induced by A oligomers (Klyubin et al.”
The amyloid hypothesis for Alzheimer’s disease: a critical reappraisal (2009, background): “…this immediately ameliorated the subtle behavioral alterations in transgenic APP animals was interpreted as indicating that this prediction had been fulfilled in animals (Janus et al. 2000; Morgan et al. 2000; Dodart et al. 2002), but as indicated above, perhaps this interpretation was premature.”
APP processing and synaptic function. (2003, neutral): “…amyloid-dependent physiological and behavioral deficits in transgenic mice can occur in the absence of cellIt is of interest, and potential clinical relevance, that inhibiting excitatory synaptic transmission or blocking death (Hsiao et al., 1996; Morgan et al., 2000; Westerman et al., 2002).”