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Elevated cerebrospinal fluid tau protein levels in Wernicke's encephalopathy
Sachio Matsushita1, Tomohiro Miyakawa, Hitoshi Maesato
1National Hospital Organization, Kurihama Alcoholism Center, Yokosuka, Kanagawa, Japan. shiguchi@wa2.so-net.ne.jp
Alcoholism, Clinical and Experimental Research
|May 1, 2008
Summary
Wernicke
Area of Science:
- Neuroscience
- Biochemistry
- Neuropathology
Background:
- Wernicke's encephalopathy (WE) neuropathology shows limited neuronal cell loss, with ongoing debate on alcohol's direct brain damage effects.
- Cerebrospinal fluid (CSF) total tau protein levels are emerging as indicators of neuronal degeneration rate in living patients.
Purpose of the Study:
- To investigate CSF total tau protein levels in patients with Wernicke's encephalopathy (WE).
- To compare CSF total tau in WE with alcohol withdrawal delirium (WD), Korsakoff syndrome (KS), and Alzheimer's disease (AD).
- To determine if elevated CSF total tau in WE reflects neuronal damage.
Main Methods:
- CSF samples were collected from patients with acute WE, WD, KS, and AD, and from chronic WE patients.
- Sandwich enzyme-linked immunosorbent assay was used to quantify CSF total tau protein levels.
- CSF levels of phosphorylated tau (p-tau(181)) and amyloid beta-protein (A beta 42) were measured for comparison with AD.
Main Results:
- Total tau was significantly elevated in acute WE, decreasing over time, but not elevated in WD or KS.
- Patterns of p-tau(181) and A beta 42 differed between acute WE and AD.
- Neuronal damage in WE appears transient and distinct from AD mechanisms.
Conclusions:
- Intense, transient neuronal cell death occurs in WE, with a mechanism distinct from Alzheimer's disease.
- Neuronal damage is typically absent in alcohol withdrawal delirium.
- CSF total tau serves as a valuable biomarker for Wernicke's encephalopathy.
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