“…Although this rodent model is far away from reproducing the complexity of the physiopathological characteristics of dementia in humans, its features may be of interest for better understanding some of the underlying mechanisms. The toxicity induced by the Ab [25][26][27][28][29][30][31][32][33][34][35] peptide in oligomeric form has been repeatedly shown to result 7 days after in neuroinflammation and reactive gliosis [18,19], pro-apoptotic caspases activity enhancement [18], oxidative stress [20], endogenously produced amyloid protein deposition [18], tau protein hyperphosphorylation [18], and increase of kinases [21,22], a reduction in the number of neurons measured in hippocampal pyramidal cell layers [17,23], loss of cholinergic neurons [24], and memory deficits [17,18,23,[25][26][27].…”