A multitude of studied synaptic proteins, located either in the pre‐synaptic terminal (e.g., synaptotagmin‐1, neuromodulin [GAP‐43], β‐synuclein, synaptosomal‐associated protein 25 [SNAP‐25]) or the post‐synaptic terminal, including neurogranin, have been shown to change their levels significantly in dementia,2, 4, 5, 6, 7, 8 prodromal disease,6, 9 and in some instances even in preclinical disease.10 This evidence concerns the gene SNAP25 and dementia.