Objective: To identify the changes of expression of p38MAPK in the olfactory bulb (OB) of rats with Alzheimer's Disease (AD) and to explore the functional mechanism of p38MAPK in the pathological changes of AD.
Methods: AD animal model was established by injecting amyloid-beta peptide 25-35 into the lateral cerebral ventricle of rats. The learning and memory abilities of rats were measured by Y-maze experiment. The expressions of p38MAPK in the OBs of rats in the AD group, saline control group, p38MAPK inhibitor group and inhibitor control (con-inhibitor) group were examined by immunohistochemistry.
Results: (1) The capabilities of learning and memory of the rats were impaired significantly at day 7 and day 14 after the induction of AD. Significant learning and memory differences were found (P < 0.05) between the AD group and the other groups. (2) The expression of p38MAPK in the OBs of rats was found at day 4 after the induction of AD. The expression increased with time. The AD rats had more positive p38MAPK cells than those in the saline controls (P < 0.05). The expression of phospho-p38MAPK in the rats with AD increased significantly (P < 0.01) compared with those in the saline group. The AD rats treated with p38MAPK inhibitor had less expression of phospho-p38MAPK than those in the AD group and the inhibitor control (P < 0.01). CONCLUSIONS; Abeta25-35 can activate p38MAPK signal transduction pathway. p38MAPK may play a role in the formation of dysosmia in AD. SB203580, a p38MAPK inhibitor, can reduce the neurotoxicity evoked by p38MAPK.