| First Author | Puzzo D | Year | 2015 |
| Journal | Neurobiol Aging | Volume | 36 |
| Issue | 4 | Pages | 1702-1715 |
| PubMed ID | 25659859 | Mgi Jnum | J:221911 |
| Mgi Id | MGI:5641824 | Doi | 10.1016/j.neurobiolaging.2015.01.004 |
| Citation | Puzzo D, et al. (2015) Role of F3/contactin expression profile in synaptic plasticity and memory in aged mice. Neurobiol Aging 36(4):1702-1715 |
| abstractText | We have recently shown that overexpression of the F3/contactin adhesive glycoprotein (also known as Contactin-1) promotes neurogenesis in adult hippocampus, which correlates with improved synaptic plasticity and memory. Because F3/contactin levels physiologically decrease with age, here, we aim at investigating whether its overexpression might counteract the cognitive decline in aged animals. For this we use 20- to 24-month-old TAG/F3 transgenic mice in which F3/contactin overexpression is driven by regulatory sequences from the gene encoding the transient axonal glycoprotein TAG-1 throughout development. We show that aged TAG/F3 mice display improved hippocampal long-term potentiation and memory compared with wild-type littermates. The same mice undergo a decrease of neuronal apoptosis at the hippocampal level, which correlated to a decrease of active caspase-3; by contrast, procaspase-3 and Bax as well as the anti-apoptotic and plasticity-related pathway BDNF/CREB/Bcl-2 were rather increased. Interestingly, amyloid-precursor protein processing was shifted toward sAPPalpha generation, with a decrease of sAPPbeta and amyloid-beta levels. Our data confirm that F3/contactin plays a role in hippocampal synaptic plasticity and memory also in aged mice, suggesting that it acts on molecular pathways related to apoptosis and amyloid-beta production. |
