MAPK8 and Senile plaques: Increases in Aβ levels remain a clear pathological mark,albeit unspecific, in the pathological development of AD, which hasbeen clearly related to neuronal stress and subsequent pathologicalperpetuator.32In vitro discoveries revealed that pJNK increases after treatment with Aβin primary cortical and hippocampal cell cultures.13−15 AD experimentalmodels have demonstrated that JNK activation is associated with increasedlevels of senile plaques.19 According tothese data in the present study, it has been demonstrated that bothAβ and pJNK increase in the familiar AD model Tg2576.