| First Author | Reyes-Marin KE | Year | 2017 |
| Journal | Brain Res | Volume | 1677 |
| Pages | 93-100 | PubMed ID | 28963050 |
| Mgi Jnum | J:268138 | Mgi Id | MGI:6270774 |
| Doi | 10.1016/j.brainres.2017.09.026 | Citation | Reyes-Marin KE, et al. (2017) Seizure susceptibility in the APP/PS1 mouse model of Alzheimer's disease and relationship with amyloid beta plaques. Brain Res 1677:93-100 |
| abstractText | Alzheimer's disease is a common age associated neurodegenerative disorder associated with an elevated risk of seizures that may be fundamentally connected to cognitive dysfunction. We used 4-9month-old mice of the APP/PS1 mouse model of Alzheimer's disease to study the presence of epileptiform-like discharges and to establish if the amyloid-beta plaques affect their generation. The EEG of the APP/PS1 transgenic mice revealed a higher incidence of epileptiform-like discharges i.e. seizure events (interictal spikes, sharp waves, or polyspikes) than in the controls. Also, APP/PS1 mice showed a lower latency to evoke seizure events than in the control animals when pentylenetetrazole (60mg/kg; i.p.) was injected. Moreover, physostigmine injection (1mg/kg; i.p.) also increased the frequency of spontaneous epileptiform-like discharges in the APP/PS1 mice. We also found a correlation between the frequency of epileptiform-like discharges and the number of amyloid-beta plaques. Application of N-(2-chloroethyl)-N-ethyl-bromobenzylamine (50mg/kg) generated amyloid-beta plaques in the cortex and seizure activity appeared. Taken together, these data indicate that deposits of amyloid-beta plaques may be responsible for the epileptiform-like discharges recorded in the APP/PS1 mice and could be responsible for the elevated risk for seizures of Alzheimer's patients. |
