Non-fibrillar β-amyloid abates spike-timing-dependent synaptic potentiation at excitatory synapses in layer 2/3 of the neocortex by targeting postsynaptic AMPA receptors

What is it about?

In this study we reported that, in addition to already known toxic effects of Aβ on classical hippocampal, tetanus-induced long-term potentiation (LTP), oligomeric Aβ abolishes spike-timing-dependent plasticity (STDP) in the neocortex by decreasing post-synaptic AMPA receptor currents. Importantly, our novel findings showed that STDP is also significantly abated in the cortex of 3.5 months-old AD mouse model, well before any cognitive disfunction or plaque formation, indicating that synaptic plasticity malfunction is an early pathological change in AD, occuring prior to main disease manifestations.

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