JNK3 overexpression, achieved by intrahippocampalinjection of an adeno-associated viral vector expressing this protein,was enough to induce cognitive deficiencies and precipitate Tau aberrantmisfolding in Tg2576 mice without accelerating amyloid pathology.JNK3 overexpression may therefore be triggered by increased Aβ.The latter, together with subsequent involvement of Tau pathology,may be underlying cognitive alterations in early stages of AD. Here, MAPT is linked to amyloidosis.