A recently proposed role for BuChE as a compensatory mechanism for AChE activity, should it become insufficient, might explain the significant increases of BuChE in contrast to no variation of AChE in hippocampus of SAMP8 with respect to SAMR1 mice, as BuChE has been proposed as a co-regulator of cholinergic transmission in neurons when strongly stimulated and exposed to high amounts of ACh [25,79] or in a pathological setting as occurs in AD [80,81]. Here, ACHE is linked to Alzheimer disease.