This makes it difficult to translate the present findings into more precise structural and functional deficits of specific forms of ChAT which could then be positively linked, taking into account their regional distribution, to AD etiopathogenesis at more intimate, i.e. molecular and cellular level (as has been done e.g. using ChAT molecular modelling in the congenital myastenic syndrome; [51–53]). The gene discussed is CHAT; the disease is Alzheimer disease.