Body to brain signalling underlies the neuro-immune pathway, but the proteins involved are incompletely characterized. Research in our lab focuses on the contribution to such signalling of human cholinesterases. In the brain, the acetylcholinesterase ACHE gene yields several protein products with different N- and C-termini. While all variants hydrolyze acetylcholine, they show different sub-cellular localizations, protein-protein interactions and physiological roles (1). Inherited and acquired changes in the expression of AChE variants and the homologous butyrylcholinesterase BChE gene induce diverse effects on the progression of Alzheimer's disease (2, 3). Moreover, antisense suppression of AChE improves myasthenia gravis symptoms (4) and facilitates the suppression of inflammation by acetylcholine. Recently, we discovered that inflammatory stimuli induce over-expression of the AChE-targeting micro-RNA-132, which is a functional regulator of the brain-to-body resolution of inflammation (5). RNA-based drugs targeting specific cholinesterases, which may have yet unknown glycosylation differences can hence open new avenues for study and therapeutic manipulations of brain-to-body communication processes.