Study About Administrating Nerve Growth Factor Intranasally Ameliorate β-Amyloid Deposition After Traumatic Brain Injury In Rats

The marked increase of amyloid-β (Aβ) peptide after traumatic brain injury (TBI), confers a risk factor for Alzheimer’s disease (AD) in patients’later life. Nerve growth factor (NGF) is great potential to repair brain injury. But its clinical application is limited because of lacking feasible methods for delivering NGF into brain. This study investigated the effects of NGF, delivered intranasally, on the Aβ burden in the central nervous system (CNS) of rats with TBI. Adult male Sprague-Dawley rats were subjected to the modified Feeney’s weight-drop model. The treatment group was treated with NGF administered by nasal route, and the control group was given phosphate-buffered saline (PBS). Beam walking and Morris water maze test were performed in the three groups. The concentration of Aβ40, Aβ42and APP in the injured ipsilateral hippocampus and cortex was elevated by ELISA measurement. Immunohistochemistry was used to detect the APP and Aβ positive cells near the region of injury in the hippocampus and cortex in rats after TBI. Western blot was performed to advance test the level of APP at7and14days following TBI. Compared to sham operated rats, TBI rats exhibited significantly increased APP and Aβ42expression as well as decreased functional outcome after TBI. Intranasal administration of NGF significantly attenuated AP42deposits, and improved functional outcome after TBI. Thus, intranasal delivery of NGF provides a potential strategy for reducing the risk of developing AD in the later life of TBI patients.