12A12mAb, when systemically (intravenously, i.v.)injected into 6-month-old Tg2576 and 3xTg mice—two AD models which respectively express the human Amyloid Precursor Protein (APP)695 with Swedish mutations (K670N-M671L), alone or in combination with MAPT P301L and PSEN1 M146V—markedly alleviates into their hippocampi the characteristic biochemical (tau hyperphosphorylation, Aβ accumulation, activation of pro-inflammatory markers), cognitive (spatial memory and orientation), electrophysiological (Long Term Potentiation, LTP induction) and morphological (spine density) alterations [57]. The gene discussed is MAPT; the disease is Alzheimer disease.