APP homodimers transduce an amyloid-β-mediated increase in release probability at excitatory synapses.

@article{Fogel2014APPHT,
  title={APP homodimers transduce an amyloid-β-mediated increase in release probability at excitatory synapses.},
  author={Hilla Fogel and Samuel Fr{\`e}re and Oshik Segev and Shashank Bharill and Ilana Shapira and Neta Gazit and Tiernan T O'Malley and Edden Slomowitz and Yevgeny Berdichevsky and Dominic M Walsh and Ehud Y Isacoff and Joel Alan Hirsch and Inna Slutsky},
  journal={Cell reports},
  year={2014},
  volume={7 5},
  pages={1560-1576}
}
Accumulation of amyloid-β peptides (Aβ), the proteolytic products of the amyloid precursor protein (APP), induces a variety of synaptic dysfunctions ranging from hyperactivity to depression that are thought to cause cognitive decline in Alzheimer's disease. While depression of synaptic transmission has been extensively studied, the mechanisms underlying synaptic hyperactivity remain unknown. Here, we show that Aβ40 monomers and dimers augment release probability through local fine-tuning of APP… CONTINUE READING
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