CaMKII Metaplasticity Drives Aβ Oligomer-Mediated Synaptotoxicity
Résumé
In Brief Opazo et al. show that oligomeric and synaptotoxic forms of the Ab peptide trigger the rapid activation of CaMKII throughout the neuron. They find that aberrant CaMKII activation leads to deficits in long-term potentiation and ultimately synaptic loss via the destabilization of AMPA receptors.
Domaines
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