Furthermore our findings on acute and potent inhibitory action exerted by pathogenetic NH2-truncated tau on glutamate release from isolated synaptosomes (Figure 4i) are also in line with the emerging concept that the unbalance in network activity occurring in vivo in prodromal AD subjects is more likely to reflect a decreased capacity of cerebral neurons to cope with existing glutamate level that becomes toxic at concentration that normally shows no harmful effect. The gene discussed is MAPT; the disease is Alzheimer disease.