| First Author | Yin XJ | Year | 2017 |
| Journal | Sci Rep | Volume | 7 |
| Pages | 40614 | PubMed ID | 28094295 |
| Mgi Jnum | J:273743 | Mgi Id | MGI:6282472 |
| Doi | 10.1038/srep40614 | Citation | Yin XJ, et al. (2017) Loss of PAFR prevents neuroinflammation and brain dysfunction after traumatic brain injury. Sci Rep 7:40614 |
| abstractText | Traumatic brain injury (TBI) is a principal cause of death and disability worldwide, which is a major public health problem. Death caused by TBI accounts for a third of all damage related illnesses, which 75% TBI occurred in low and middle income countries. With the increasing use of motor vehicles, the incidence of TBI has been at a high level. The abnormal brain functions of TBI patients often show the acute and long-term neurological dysfunction, which mainly associated with the pathological process of malignant brain edema and neuroinflammation in the brain. Owing to the neuroinflammation lasts for months or even years after TBI, which is a pivotal causative factor that give rise to neurodegenerative disease at late stage of TBI. Studies have shown that platelet activating factor (PAF) inducing inflammatory reaction after TBI could not be ignored. The morphological and behavioral abnormalities after TBI in wild type mice are rescued by general knockout of PAFR gene that neuroinflammation responses and cognitive ability are improved. Our results thus define a key inflammatory molecule PAF that participates in the neuroinflammation and helps bring about cerebral dysfunction during the TBI acute phase. |
