In this connection our data, showing that 12A12mAb treatment in vivo enhances the structural plasticity and permits a functional recovery of neural circuits by normalizing the dysregulation of actin dynamics in the primary visual cortex, are much more consistent with the hypothesis that the neurotoxic N-truncated tau in the Tg2576 AD mouse model locally engages signaling pathways for dendritic spine loss by inducing the ADF/cofilin dephosphorylation, as previously reported in their hippocampi [42]. This evidence concerns the gene MAPT and Alzheimer disease.