| First Author | Chen C | Year | 2018 |
| Journal | Ann Clin Transl Neurol | Volume | 5 |
| Issue | 8 | Pages | 982-987 |
| PubMed ID | 30128323 | Mgi Jnum | J:264801 |
| Mgi Id | MGI:6198867 | Doi | 10.1002/acn3.599 |
| Citation | Chen C, et al. (2018) Mapt deletion fails to rescue premature lethality in two models of sodium channel epilepsy. Ann Clin Transl Neurol 5(8):982-987 |
| abstractText | Deletion of Mapt, encoding the microtubule-binding protein Tau, prevents disease in multiple genetic models of hyperexcitability. To investigate whether the effect of Tau depletion is generalizable across multiple sodium channel gene-linked models of epilepsy, we examined the Scn1b(-/-) mouse model of Dravet syndrome, and the Scn8a(N1768D/+) model of Early Infantile Epileptic Encephalopathy. Both models display severe seizures and early mortality. We found no prolongation of survival between Scn1b(-/-),Mapt(+/+) , Scn1b(-/-),Mapt(+/-,) or Scn1b(-/-),Mapt(-/-) mice or between Scn8a(N1768D/+),Mapt(+/+) , Scn8a(N1768D/+),Mapt(+/-) , or Scn8a(N1768D/+),Mapt(-/-) mice. Thus, the effect of Mapt deletion on mortality in epileptic encephalopathy models is gene specific and provides further mechanistic insight. |
