| First Author | Murphy M | Year | 2015 |
| Journal | Neurobiol Aging | Volume | 36 |
| Issue | 2 | Pages | 740-52 |
| PubMed ID | 25443284 | Mgi Jnum | J:219519 |
| Mgi Id | MGI:5621099 | Doi | 10.1016/j.neurobiolaging.2014.09.014 |
| Citation | Murphy M, et al. (2015) Reduction of p75 neurotrophin receptor ameliorates the cognitive deficits in a model of Alzheimer's disease. Neurobiol Aging 36(2):740-52 |
| abstractText | Alzheimer's disease (AD) is an extremely prevalent cause of dementia. It is characterized by progressive memory loss, confusion, and other behavioral and physiological problems. The amyloid-beta (Abeta) protein is thought to be involved in the pathogenesis of AD, and there is evidence that Abeta may act through the p75 neurotrophin receptor (p75) to mediate its pathogenic effects. This raises the possibility that reducing levels of p75 could be a treatment for AD by preventing the effects of Abeta. In this study, we have crossed the transgenic AD model mice, Tg2576, with p75(-/-) mice to generate Tg2576/p75(+/-) mice with reduced levels of p75. These mice are rescued from the deficits in learning and memory and hippocampal function which were found in the Tg2576 mice. These findings suggest that reduction of p75 can ameliorate some of the primary symptoms of AD. |
