Accumulating evidence suggests that butyrylcholinesterase (BuChE) plays an important role in the progression of cognitive deficits and Alzheimer-type pathology in dementia patients. We examined the relationship between the K variant of BuChE and the severity of deposits of amyloid (Aβ1–42) and phosphorylated tau in the temporal cortex (BA36) of 30 prospectively studied autopsy-diagnosed dementia (Alzheimer’s disease and dementia with Lewy bodies) patients. There was 42% less phosphorylated tau in BA36 in cases with ≧1 K compared with those with wild-type BuChE alleles (t = 2.2, p = 0.039), but no difference in the extent of Aβ1–42 deposition. BuChE may play this role in the phosphorylation of tau, relevant to therapeutic inhibition of the enzyme.

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