Soluble oligomers of the amyloid beta-protein impair synaptic plasticity and behavior.

By D. Selkoe. Behavioural Brain Research, 2008

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Protection of synapses against Alzheimer's-linked toxins: Insulin signaling prevents the pathogenic binding of Aβ oligomers (2009, background): “The attack on synapses inhibits long-term potentiation (LTP) (11, 13, 14), a classic paradigm for memory-related synaptic mechanisms.”
Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012, background): “Abundant evidence from many independent studies indicates that A A peptides and other plaque substances (in their various molecular forms) may be neuro-toxic, both directly and through secondary responses to stress, injury, and inﬂammation (46, 82, 83).”
Identification of Amyloid Plaques in Retinas from Alzheimer’s Patients and Noninvasive In Vivo Optical Imaging of Retinal Plaques in a Mouse Model (2010, neutral): “To further verify the specificity of curcumin-labeled Aβ plaques in the human retina, we used 11A5-B10 and 12F4 mAbs recognizing the C-terminal Aβ 40 and Aβ 42 forms, respectively, found to be elevated in brains of AD patients (Selkoe, 2008).”