While we cannot totally rule out a potential lack of sensitivity of 18F-IAM6067 in our experimental settings, the absence of decreases in S1R binding in the mouse PD model and AD brains, the increase in the substantia nigra in the AMPA model in rats (Supplementary Figure 1A & B), taken together with previous reports 17, 18, 20, 67, 68 suggest that S1R expression and/or binding characteristics are altered differently in different population of neurons or depending on the paradigms. The gene discussed is TMBIM4; the disease is Alzheimer disease.