To address the question whether increased amyloid-β load facilitates post-traumatic epileptogenesis we induced traumatic brain injury (TBI) in 13–15 week old APP/PS1 mice and Wt littermates. Gene expression profiling of perilesional cortex, ipsilateral thalamus and hippocampus was performed using Affymetrix microarray system. APP/PS1 injured mice showed motor deficits compared to APP/PS1 controls (P<0.01) and Wt injured mice (P<0.01) in Neuroscore. Latency to find the platform in Morris water-maze was longer in APP/PS1 injured mice than in Wt injured group (P<0.05). Probe trial showed impaired spatial memory in APP/PS1 injured mice compared to APP/PS1 controls (P<0.05). Video-EEG monitoring (24 h/7 days, 2 week) performed at 6 week post-TBI revealed spontaneous seizures in 86% of APP/PS1 injured mice and 36% of APP/PS1 controls (P<0.05). None of Wt controls and 7% of Wt injured mice displayed spontaneous seizures (P<0.01 compared to APP/PS1 injured mice). Video-EEG monitoring (24 h/7 days, 2 week) starting at 14 week post-TBI showed spontaneous seizures in 50% of APP/PS1 injured mice and 13% of APP/PS1 controls (P>0.05). Neither Wt injured mice nor Wt controls had spontaneous seizures. Microarray data analysis revealed changes in transcriptome between groups. Enhanced amyloidogenesis results in more pronounced epileptogenesis and more severe motor and cognitive co-morbidities following TBI.
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.