In view of the key roles played by both RyR and BDNF in synaptic plasticity [92,94,97,98,99], our findings that AβOs interrupt GBZ-induced nuclear Ca2+ signals and the ensuing expression of both BDNF and RyR2 mRNA levels, may add to our current understanding of AD pathology. The gene discussed is BDNF; the disease is Alzheimer disease.