Based on all the above-mentioned data, the aim of the presentworkis to study the expression of JNK in AD brains compared to other dementingneurodegenerative entities and its relationship with Aβ pathology.Moreover, the consequences on cognitive performance, amyloid burden,and Tau pathology of JNK3 overexpression in a transgenic mouse modelwere studied to elucidate whether JNK overactivation is a cause ora consequence of Aβ accumulation. This evidence concerns the gene MAPK10 and Alzheimer disease.