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Bliss TV, Collingridge GL (1993) A synaptic model of memory: long-term potentiation in the hippocampus. Nature 361(6407):31–39.
Chapman PF, White GL, et al. (1999) Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice. Nat Neurosci 2(3):271–276.
Chen QS, Wei WZ, et al. (2002) Alzheimer amyloid beta-peptide inhibits the late phase of long-term potentiation through calcineurin-dependent mechanisms in the hippocampal dentate gyrus. Neurobiol Learn Mem 77(3):354–371.
Cullen WK, Suh YH, et al. (1997) Block of LTP in rat hippocampus in vivo by beta-amyloid precursor protein fragments. Neuroreport 8(15):3213–3217.
Hsia AY, Masliah E, et al. (1999) Plaque-independent disruption of neural circuits in Alzheimer’s disease mouse models. Proc Natl Acad Sci USA 96(6):3228–3233.
Kamenetz F, Tomita T, et al. (2003) APP processing and synaptic function. Neuron 37(6):925–937.
Lambert MP, Barlow AK, et al. (1998) Diffusible, nonfibrillar ligands derived from Abeta1-42 are potent central nervous system neurotoxins. Proc Natl Acad Sci USA 95(11):6448–6453.
Larson J, Lynch G, et al. (1999) Alterations in synaptic transmission and long-term potentiation in hippocampal slices from young and aged PDAPP mice. Brain Res 840(1–2):23–35.
Moechars D, Dewachter I, et al. (1999) Early phenotypic changes in transgenic mice that over-express different mutants of amyloid precursor protein in brain. J Biol Chem 274(10):6483–6492.
Morishita W, Marie H, et al. (2005) Distinct triggering and expression mechanisms underlie LTD of AMPA and NMDA synaptic responses. Nat Neurosci 8(8):1043–1050.
Selkoe DJ (2001) Alzheimer’s disease:genes, proteins, and therapy. Physiol Rev 81(2):741–766.
Snyder EM, Nong Y, et al. (2005) Regulation of NMDA receptor trafficking by amyloid-beta. Nat Neurosci 8(8):1051–1058.
Stern EA, Bacskai BJ, et al. (2004) Cortical synaptic integration in vivo is disrupted by amyloidbeta plaques. J Neurosci 24(19):4535–4540.
Terry RD, Masliah E, et al. (1991) Physical basis of cognitive alterations in Alzheimer’s disease:synapse loss is the major correlate of cognitive impairment. Ann Neurol 30(4):572–580.
Walsh DM, Klyubin I, et al. (2002) Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo. Nature 416(6880):535–539.
Wang Q, Rowan MJ, et al. (2004) Beta-amyloid-mediated inhibition of NMDA receptor-dependent long-term potentiation induction involves activation of microglia and stimulation of inducible nitric oxide synthase and superoxide. J Neurosci 24(27):6049–6056.
Wu J, Anwyl R, et al. (1995) beta-Amyloid selectively augments NMDA receptor-mediated synaptic transmission in rat hippocampus. Neuroreport 6(17):2409–2413.
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Malinow, R., Hsieh, H., Wei, W. (2007). Beta Amyloid and Excitatory Synapses. In: Sisodia, S.S., Tanzi, R.E. (eds) Alzheimer’s Disease. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-35135-3_9
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DOI: https://doi.org/10.1007/978-0-387-35135-3_9
Publisher Name: Springer, Boston, MA
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