| First Author | Zhao Y | Year | 2017 |
| Journal | Neuron | Volume | 96 |
| Issue | 2 | Pages | 355-372.e6 |
| PubMed ID | 29024660 | Mgi Jnum | J:253213 |
| Mgi Id | MGI:6109630 | Doi | 10.1016/j.neuron.2017.09.041 |
| Citation | Zhao Y, et al. (2017) Amyloid Beta Peptides Block New Synapse Assembly by Nogo Receptor-Mediated Inhibition of T-Type Calcium Channels. Neuron 96(2):355-372.e6 |
| abstractText | Compelling evidence links amyloid beta (Abeta) peptide accumulation in the brains of Alzheimer''s disease (AD) patients with the emergence of learning and memory deficits, yet a clear understanding of the events that drive this synaptic pathology are lacking. We present evidence that neurons exposed to Abeta are unable to form new synapses, resulting in learning deficits in vivo. We demonstrate the Nogo receptor family (NgR1-3) acts as Abeta receptors mediating an inhibition of synapse assembly, plasticity, and learning. Live imaging studies reveal Abeta activates NgRs on the dendritic shaft of neurons, triggering an inhibition of calcium signaling. We define T-type calcium channels as a target of Abeta-NgR signaling, mediating Abeta''s inhibitory effects on calcium, synapse assembly, plasticity, and learning. These studies highlight deficits in new synapse assembly as a potential initiator of cognitive pathology in AD, and pinpoint calcium dysregulation mediated by NgRs and T-type channels as key components. VIDEO ABSTRACT. |
