| First Author | Del Vecchio RA | Year | 2004 |
| Journal | Neurosci Lett | Volume | 367 |
| Issue | 2 | Pages | 164-7 |
| PubMed ID | 15331144 | Mgi Jnum | J:101573 |
| Mgi Id | MGI:3604276 | Doi | 10.1016/j.neulet.2004.05.107 |
| Citation | Del Vecchio RA, et al. (2004) Increased seizure threshold and severity in young transgenic CRND8 mice. Neurosci Lett 367(2):164-7 |
| abstractText | Reports suggest that Alzheimer's disease (AD) patients show a high life-time prevalence of seizure-like disorders. The transgenic CRND8 (TgCRDN8) is a mouse model of AD-like amyloid pathogenesis that expresses a double-mutant form of human amyloid precursor protein 695 (K670N/M671L and V717F). We have previously reported that post-plaque TgCRND8 mice exhibited a lower threshold to seizure with a more severe seizure type when challenged with pentylenetetrazole (PTZ) intravenously. Here, we now report that pre-plaque TgCRND8 mice also demonstrate an increased sensitivity to PTZ-induced seizures with a more severe seizure type over age-matched littermate controls. A lower threshold and more severe seizure type in TgCRND8 mice prior to and after plaque deposition suggest that this genotype difference may be due to beta-amyloid (Abeta) toxicity rather than plaque formation. Thus, the TgCRND8 mice are not only a model for Abeta production and plaque deposition, but may also be useful for AD associated seizure. |
