Abstract
A recently described triple-transgenic mouse model (3×Tg, PS1 M146V, APP Swe, and tau P301L) develops a neuropathology similar to the brains of Alzheimer’s disease patients including progressive deposits of plaques and tangles [Neuron 39 (2003) 409]. These mice also show age-related deficits in hippocampal synaptic plasticity that occurs before the development of plaques and tangles. Here we report unchanged synaptic vesicle recycling, as measured by FM1-43 release, in the hippocampal neurons of the 3×Tg mice. Expression levels of presynaptic protein synaptophysin and of proteins involved in synaptic vesicle recycling including AP180, dynamin I, and synaptotagmin I also remain unaffected. These data suggest that the synaptic deficits observed in the 3×Tg neurons may not arise from the preserved synaptic vesicle recycling.
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More From: Biochemical and Biophysical Research Communications
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