Taking these known functions of nAChR and SLURPs into account, the absence of NNCS markers in non-lesional AD skin observed here and specifically the lack of α7nAChR in lesional AD skin may relate to the thickened epidermis characterized by dysfunctional cell differentiation [37] and to a shortage of anti-inflammatory effects normally provided by the NNCS. Here, CHRNA7 is linked to Alzheimer disease.