PI3K Activation Prevents Aβ42-induced Synapse Loss and Favors Insoluble Amyloid Deposit Formation

The toxic effects of human Aβ42 peptide on synapses can be prevented by PI3K activation. This neuroprotection is achieved by increasing the insoluble aggregates of the peptide through the PI3K-triggered phosphorylation of the Ser-26 residue in Aβ42. The Aβ42 toxicity syndrome includes the abrogation of PI3K expression.