Elevated cerebrospinal fluid tau protein levels in Wernicke's encephalopathy

Sachio Matsushita, Tomohiro Miyakawa, Hitoshi Maesato, Toshifumi Matsui, Akira Yokoyama, Hiroyuki Arai, Susumu Higuchi, Haruo Kashima

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)

Abstract

Objective: Limited neuronal cell loss is seen in the neuropathology of Wernicke's 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 Alzheimer's disease (AD) as a disease control. Methods: 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 enzyme-linked immunosorbent assay. Tau phosphorylated at threonine 181 (p-tau181) and amyloid β-protein ending at amino acid 42 (Aβ42) in CSF were also determined for comparison between acute WE with AD. Results: Total tau was significantly elevated in acute WE and decreased on long-term follow-up, but was not elevated in WD or KS. The patterns of p-tau181 and Aβ42 differed between acute WE and AD. Conclusions: 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.

Original languageEnglish
Pages (from-to)1091-1095
Number of pages5
JournalAlcoholism: Clinical and Experimental Research
Volume32
Issue number6
DOIs
Publication statusPublished - 2008 Jun

Keywords

  • Alcohol Withdrawal Delirium
  • Cerebrospinal Fluid
  • Korsakoff Syndrome
  • Tau Protein
  • Wernicke's Encephalopathy

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Toxicology
  • Psychiatry and Mental health

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