Apart from the Aβ induced pathology, they also display neuroinflammation, synaptic alterations with age and genotype dependent progressive cognitive impairment.29,34,46 Studies in the Tg2576 and the 5xFAD transgenic mouse models of Alzheimer’s disease, have also reported reduced presynaptic and postsynaptic markers such as synaptophysin and PSD-95 at a similar extent as in App knock-in models.34,47,48 Faster disease progression models are more cost effective and thus often favoured in the field. The gene discussed is DLG4; the disease is early-onset autosomal dominant Alzheimer disease.