Conversely, the expression level of two major postsynaptic proteins -N-Methyl-D-aspartate (NMDA) Receptor subunit NR1 and postsynaptic density protein 95 (PSD95) - did not change or even significantly increased, likely due to reactive/compensatory mechanisms reminiscent of those occurring in vivo during progression of AD pathology [83, 84]. Here, DLG4 is linked to Alzheimer disease.