Of course, more detailed studies are required to address whether this NR2A-mediated reduction in GSK3β activity could also be important for limiting the progression of other cellular damages (particularly liposomal dysfunctions) which are associated with Alzheimer's disease [57], and further studies are definitely necessary to elucidate whether the NR2A/PKC/GSK3β pathway may provide novel perspectives for the treatment of excitotoxicity in pathologies such as ischemic stroke. This evidence concerns the gene PRRT2 and early-onset autosomal dominant Alzheimer disease.