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clinmed/2001110002v1 (December 17, 2001)
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Amyloid plaque (and not diffuse amyloid) is a condition for neuronal dysfunction

Alexei R. Koudinov, Temirbolat T. Berezov, and Natalia V. Koudinova

There is no direct evidence that brain amyloid affects neuronal function. In this report we studied hippocampal slices from non-mutated human amyloid precursor protein (APP695) transgenic- and age-matched non-transgenic control mice. We aimed to differentiate separate actions of the aged (25.5 months) transgenic mice plaque-like amyloid and diffuse amyloid of the non-transgenic mice (verified by immunohistochemistry and Congo Red fluorescence) on synaptic plasticity. Extracellular recording of CA1 field excitatory postsynaptic potentials in vitro revealed impairment of input/output characteristics, long-term potentiation, and the delay of few milliseconds in initial post-tetanic traces in aged transgenic versus control mice hippocampal slices. Our results indicate that amyloid plaque (and not diffuse amyloid) may cause synaptic dysfunction, and suggest importance factors other then brain amyloid in pre-plaque stages of Alzheimer’s disease and in Down syndrome.

E.mail contact: koudin{at}imb.ac.ru or amyloidbeta{at}hotmail.com

Key words: Alzheimer's disease, amyloid beta protein precursor, cholesterol, Down syndrome, etiology, extracellular recording, EPSP, hippocampus, learning, lipid, long term potentiation and depression, LTP, LTD, memory, neurodegeneration marker, neurofilament, oxidative stress cascade, PHF NFT tau phosphorylation, phospholipids, plaque, secretase, synaptic plasticity, therapy





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