“…Mouse AD models were, either non-transgenic [ 35 , 36 ], where mice’s brains were injected with a high concentration of Aβ1-42, or transgenic, most frequently used were the APP/PS1 double transgenic mice [ 11 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 ]. Rat models of AD, to study NPs effect on memory dysfunction, were all non-transgenic (most often adult Wistar rats), where AD-like brain pathology was elicited by exposing the animals brain to high concentrations of either Aβ1-40 [ 44 ], Aβ1-42 [ 51 , 52 , 53 ], β-amyloid proteins [ 32 ], STZ [ 31 , 56 , 57 ], scopolamine [ 33 ], okadaic acid [ 13 ] or AlCl 3 [ 34 ]. Molecular pathways of amyloid and tau pathology, where NPs’ treatment attenuated memory dysfunction in AD model animals are summarised in Figure 2 .…”