elevated cerebrospinal fluid tau protein levels in wernickes encephalopathy objective limited neuronal cell loss is seen in the neuropathology of wernickes encephalopathy we but the extent of neuronal damage has not been well studied moreover there is still a debate as to whether alcohol itself causes brain damage in humans although it is difficult to examine the extent of neuronal damage in living patients recent studies have revealed that total tau protein levels in the cerebrospinal fluid csf reflect the rate of neuronal degeneration therefore we hypothesized that the elevated csf total tau in patients with we was due to neuronal damage and thus we examined csf total tau protein in patients with we as well as in those with alcohol withdrawal delirium wd and korsakoff syndrome ks we also examined csf total tau in nonalcohol dependent patients with alzheimers disease ad as a disease controlmethods csf samples were obtained from 13 acute we patients with alcohol dependence 9 wd patients with alcohol dependence and 16 ks patients with alcohol dependence and from 20 nonalcohol dependent ad patients csf was also obtained from 10 of the we patients after their disease had progressed to the chronic stage csf tau protein levels in all samples were determined by sandwich enzymelinked immunosorbent assay tau phosphorylated at threonine 181 ptau181 and amyloid betaprotein ending at amino acid 42 a beta 42 in csf were also determined for comparison between acute we with adresults total tau was significantly elevated in acute we and decreased on longterm followup but was not elevated in wd or ks the patterns of ptau181 and a beta 42 differed between acute we and adconclusions intense neuronal cell death occurs transiently in we and the mechanism differs from that in ad neuronal damage is generally unaccompanied in wd these results suggest that csf total tau is a useful biological marker for we