If, as we assert here, loss of function is a key part of etiology towards neuron death and dementia, then this has significance in two applied areas: (1) preventing loss of function may be a therapeutic strategy; (2) promising therapeutic strategies that seek to reduce PrPC abundance in order to prevent disease progression may be ill-fated, or perhaps can be improved upon by considering strategies to ameliorate disease-promoting effects of their loss of function. Here, PRNP is linked to dementia.