Soluble amyloid beta peptide (Abeta) is believed to cause synaptic dysfunction in the early stages of Alzheimer's disease. Here, we examined in-vivo synaptic functions in the hippocampus in two lines of transgenic mice expressing different amounts of human wild-type amyloid precursor protein (APP). Compared with nontransgenic littermates, one transgenic line with higher APP expression displayed potent inhibition of paired-pulse facilitation and long-term potentiation in the absence of amyloid deposition, whereas the line with lower APP expression exhibited moderate inhibition of paired-pulse facilitation and long-term potentiation. Soluble Abeta1-42 levels in their brains nearly paralleled APP levels. The observed inverse correlation between APP expression and synaptic plasticity appears to support the current hypothesis regarding the pathogenic roles of soluble Abeta.
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