“…One of the main clinical outcomes of AD, other than memory impairment and cognitive decline, is seizure: in fact, AD patients suffer from a higher incidence of seizure (Amatniek et al, 2006 ). In relation to this clinical observation, recent work was conducted in our and other labs, focusing on the characterization of the disruption of hippocampal and cortical neuronal synchronized activity in models of AD (Palop et al, 2007 ; Minkeviciene et al, 2009 ; Putcha et al, 2011 ; Verret, 2012 ; Corbett et al, 2013 ; Born et al, 2014 ; Davis et al, 2014 ); further research efforts were also spent on the characterization of the intrinsic excitability (IE) alterations of neuronal properties in mouse models of amyloidopathy, such as PSAPP (Brown et al, 2011 ), PDAPP (Kerrigan et al, 2014 ), CRND8 (Wykes et al, 2012 ), 5xFAD (Kaczorowski et al, 2011 ), APPSwe/PS1dE9 (Kellner et al, 2014 ), soluble oligomers of Aβ 1–42 (Scala et al, 2015 ; Tamagnini et al, 2015 ), 3xTg APPSwe/PS1/P301L (Scala et al, 2015 ), Tg2576 (Brown et al, 2011 ; Nenov et al, 2015 ) and APP23xPS45 (Busche et al, 2012 ).…”