| First Author | Li S | Year | 2013 |
| Journal | Neuron | Volume | 77 |
| Issue | 5 | Pages | 929-41 |
| PubMed ID | 23473322 | Mgi Jnum | J:197937 |
| Mgi Id | MGI:5494918 | Doi | 10.1016/j.neuron.2012.12.040 |
| Citation | Li S, et al. (2013) Environmental novelty activates beta2-adrenergic signaling to prevent the impairment of hippocampal LTP by Abeta oligomers. Neuron 77(5):929-41 |
| abstractText | A central question about human brain aging is whether cognitive enrichment slows the development of Alzheimer changes. Here, we show that prolonged exposure to an enriched environment (EE) facilitated signaling in the hippocampus of wild-type mice that promoted long-term potentiation. A key feature of the EE effect was activation of beta2-adrenergic receptors and downstream cAMP/PKA signaling. This EE pathway prevented LTP inhibition by soluble oligomers of amyloid beta-protein (Abeta) isolated from AD cortex. Protection by EE occurred in both young and middle-aged wild-type mice. Exposure to novelty afforded greater protection than did aerobic exercise. Mice chronically fed a beta-adrenergic agonist without EE were protected from hippocampal impairment by Abeta oligomers. Thus, EE enhances hippocampal synaptic plasticity by activating beta-adrenoceptor signaling and mitigating synaptotoxicity of human Abeta oligomers. These mechanistic insights support using prolonged exposure to cognitive novelty and/or oral beta-adrenergic agonists to lessen the effects of Abeta accumulation during aging. |
