title: Intranasal administration of nerve growth factor ameliorate β-amyloid deposition after traumatic brain injury in rats.
abstract: 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 injured ipsilateral cortex and hippocampus of rats with TBI. Adult male Sprague-Dawley rats were subjected to the modified Feeney's weight-drop model and treated without or with NGF by intranasal route. Motor and cognitive functional outcome, immunostaining, ELISA assay and western blot were performed. Compared to sham operated rats, TBI rats exhibited significantly increased APP and Aβ₄₂ expression as well as decreased functional outcome after TBI. Intranasal administration of NGF significantly attenuated Aβ₄₂ deposits, 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.
authors.affiliation: Department of Neurology, Jinling Hospital, Nanjing University School of Medicine, 305 East Zhongshan Road, Nanjing 210002, Jiangsu Province, China.
authors.forename: Lili
authors.initials: L
authors.lastname: Tian
authors.forename: Ruibing
authors.initials: R
authors.lastname: Guo
authors.forename: Xuanye
authors.initials: X
authors.lastname: Yue
authors.forename: Qiushi
authors.initials: Q
authors.lastname: Lv
authors.forename: Xinchun
authors.initials: X
authors.lastname: Ye
authors.forename: Zhenzhen
authors.initials: Z
authors.lastname: Wang
authors.forename: Zhaoyao
authors.initials: Z
authors.lastname: Chen
authors.forename: Bo
authors.initials: B
authors.lastname: Wu
authors.forename: Gelin
authors.initials: G
authors.lastname: Xu
authors.forename: Xinfeng
authors.initials: X
authors.lastname: Liu
mesh_terms: D000281:Administration, Intranasal; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism*; D000818:Animals; D001930:Brain Injuries / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D002540:Cerebral Cortex / Q000187:drug effects* / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D018782:Maze Learning / Q000187:drug effects; D009043:Motor Activity / Q000187:drug effects; D020932:Nerve Growth Factor / Q000008:administration & dosage*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D010446:Peptide Fragments / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42); D020932:Nerve Growth Factor