A direct interaction between Hsp60 and pre-formed oligomeric species of Aβ1–42 (oAβs) has been further demonstrated by in vitro and ex vivo experiments, showing that Hsp60 treatment was able to: (i) block the oAβs toxic effect in neuroblastoma cells (SH-SY5Y), (ii) significantly reduce the oAβ-driven impairment of long-term potentiation (LTP) and synaptic plasticity in mouse hippocampal brain slices using ex vivo field electrophysiology [37]. This evidence concerns the gene HSPD1 and neuroblastoma.