Recently, reports suggest that increased levels of eIF2α phosphorylation observed in transgenic mouse models of Alzheimer’s disease and frontotemporal dementia and mice with prion disease amplifies neurodegeneration and defects in synaptic function (Devi and Ohno, 2014; Ma et al., 2013; Moreno et al., 2012; Radford et al., 2015; Segev et al., 2015), although other studies have failed to confirm some of these findings (Devi and Ohno, 2013; Paesler et al., 2015; Sadleir et al., 2014). Here, EIF2A is linked to frontotemporal dementia.