Elevated Cerebrospinal Fluid Tau Protein Levels in Wernicke’s Encephalopathy

Matsushita, Satoru; Miyakawa, Tsuyoshi; Maesato, Hitoshi; Matsui, Toshifumi; Yokoyama, Akira; Arai, Hiroyuki; Higuchi, Susumu; Kashima, Haruo

doi:10.1111/j.1530-0277.2008.00671.x

Cited by 22 publications

(22 citation statements)

References 25 publications

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“…TD increases the activity of brain b-secretase and oxidative stress and exacerbates cerebral b-amyloid (Ab) deposition in APP/PS1 transgenic mice (Karuppagounder et al 2009;Zhang et al 2009). Furthermore, patients with Wernicke's encephalopathy induced by TD have been observed to have elevated phosphorylated Tau levels in their cerebrospinal fluid (CSF) (Matsushita et al 2008), which is also seen in AD patients. Thus, TD may contribute to the pathogenesis of AD.…”

Section: Introductionmentioning

confidence: 99%

Exposure to Pyrithiamine Increases β-Amyloid Accumulation, Tau Hyperphosphorylation, and Glycogen Synthase Kinase-3 Activity in the Brain

Zhao

Sun

et al. 2010

Neurotox Res

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Decreased thiamine-dependent enzyme activity and/or thiamine deficiency (TD) have been linked to Alzheimer's disease (AD). In this study, we administered pyrithiamine, an anti-thiamine compound, to both APP/PS1 transgenic mice and wild-type littermate control mice; alternatively, we induced TD by thiamine-depleted diet. Pyrithiamine treatment and diet-induced TD impaired the memory of wild-type mice, but had little effect on APP/PS1 mice. Pathophysiologically, pyrithiamine treatment and diet-induced TD aggravated β-amyloid accumulation in the brain. This was demonstrated by increased β-amyloid in the brains of wild-type mice using ELISA and by the number of amyloid plaques in the brains of APP/PS1 transgenic mice using immunochemical staining. Also, enhanced numbers of phosphorylated Tau-positive cells were observed in both APP/PS1 transgenic and wild-type mice. Furthermore, pyrithiamine decreased the phosphorylation rates of glycogen synthase kinase (GSK)-3β and raised its enzymatic activity, but had little influence on GSK-3α. Diet-induced TD reduced the phosphorylated rates and increased the activities of GSK-3, GSK-3α, and GSK-3β. These results suggest that when sufficient thiamine supplement is administered, pyrithiamine can cause AD-like pathological alterations similar to that of diet-induced TD.

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Section: Introductionmentioning

confidence: 99%

Exposure to Pyrithiamine Increases β-Amyloid Accumulation, Tau Hyperphosphorylation, and Glycogen Synthase Kinase-3 Activity in the Brain

Zhao

Sun

et al. 2010

Neurotox Res

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“…Matsushita et al 6 describe a case series of acute WE in alcohol-dependent subjects and found elevated CSF tau level in all of them. The mean level of CSF tau was 1069 and the highest level found was 1995 ng/l.…”

Section: Discussionmentioning

confidence: 99%

“…In recent years, we have seen a rapid increase in the number of studies being published on CSF tau in Alzheimer's disease (AD)4 5 and other dementia syndromes 6. CSF tau has been proposed as a general marker for neuronal degeneration 7.…”

Section: Discussionmentioning

confidence: 99%

Elevated cerebrospinal fluid tau in Wernicke encephalopathy

2012

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SummaryWernicke encephalopathy (WE) commonly presents with oculomotor abnormalities, gait ataxia and confusion. WE can mimic rapidly progressive dementia syndromes, such as Creutzfeldt-Jakob disease (CJD). Cerebrospinal fluid (CSF) tau is frequently used for diagnosis of several dementia subtypes, predominantly CJD and Alzheimer's disease. The combination of very high CSF tau (tau) and normal phosphorylated tau ( p-tau) levels is almost exclusively seen in aggressive diseases, such as CJD. The authors present a case of a woman with WE, caused by chronic insufficient dietary intake, with highly elevated CSF tau and normal p-tau. The clinical symptoms and CSF findings raised the suspicion of CJD. However, shortly after immediate treatment with thiamine the patient clinically improved. At followup, 2.5 months later, she had made a good recovery. This case of rapidly progressive dementia illustrates that, even in the case of a highly elevated CSF tau, clinicians should be alert for treatable causes such as WE. BACKGROUND

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“…Elevated values for CSF-tTau have also been found in a bovine variant of CJD [104]. Increases of CSF-tTau levels are observed in several other acute neurological conditions, such as severe malaria [105], Wernicke's encephalopathy [106], pediatric patients with brain tumor, hydrocephalus or serious CNS infections [107]. Studies assessing CSF-tTau in non-AD dementia such as FTD, PSP, CBD, Lewy body dementia (LBD), Parkinson's disease dementia (PDD) and amyotrophic lateral sclerosis (ALS) give contradictory results.…”

Section: Csf Total Tau: a Biomarker Of Neuronal Degenerationmentioning

confidence: 94%

“…The use of phosphodependent antibodies showed that pTau is recovered in the CSF and that several phosphoepitopes are present [98], [184] 192 AD 1 year 21% CV 21% CV NA NA [185] 29 AD 2 years 548 ± 355 577 ± 275 NA NA [186] 8 MCI 1 year 530 ± 450 560 ± 480 [146] 20 AD 3-8 years 568 ± 365 570 ± 435 NA NA [130] 53 AD 6 months 425 ± 30 431 ± 30 (6.1% CV) 93 ± 6 94 ± 6 (4.4% CV) [187] 50 AD 21 ± 8 months 731 ± 363 791 ± 419 84 ± 34 85 ± 35 [161] 22 MCI-AD 2.1 ± 0.5 years 750 ± 553 667 ± 327 49 ± 31 52 ± 29 [150] 12 MCI-AD 2 years 700 (240-1700) 710 (270 -1300) 86 86 (48-150) [156] 66 CJD 6 weeks tTau not significant tTau not significant NA NA [188] Transient increase in CSF-tTau and pTau levels in conditions with neuronal/axonal loss [190] Alcoholic dementia CSF-Tau/pTau significantly elevated in acute WE (n = 10) but not in chronic WE and after long-term follow-up [106] AD such as Thr181, Thr235, Ser396 and Ser404. A moderate to marked increase in CSF-pTau compared with controls has been found for all the different ELISA methods based on these antibodies [98,99].…”

Section: Csf-ptau: a Biomarker Of Hyperphosphorylationmentioning

confidence: 94%

Tau as a Biomarker of Neurodegenerative Diseases

et al. 2008

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The microtubule-associated protein Tau is mainly expressed in neurons of the CNS and is crucial in axonal maintenance and axonal transport. The rationale for Tau as a biomarker of neurodegenerative diseases is that it is a major component of abnormal intraneuronal aggregates observed in numerous tauopathies, including Alzheimer's disease. The molecular diversity of Tau is very useful when analyzing it in the brain or in the peripheral fluids. Immunohistochemical and biochemical characterization of Tau aggregates in the brain allows the postmortem classification and differential diagnosis of tauopathies. As peripheral biomarkers of Alzheimer's disease in the cerebrospinal fluid, Tau proteins are now validated for diagnosis and predictive purposes. For the future, the detailed characterization of Tau in the brain and in peripheral fluids will lead to novel promising biomarkers for differential diagnosis of dementia and monitoring of therapeutics.

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Elevated Cerebrospinal Fluid Tau Protein Levels in Wernicke’s Encephalopathy

Abstract: 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.

Cited by 22 publications

References 25 publications

Exposure to Pyrithiamine Increases β-Amyloid Accumulation, Tau Hyperphosphorylation, and Glycogen Synthase Kinase-3 Activity in the Brain

Exposure to Pyrithiamine Increases β-Amyloid Accumulation, Tau Hyperphosphorylation, and Glycogen Synthase Kinase-3 Activity in the Brain

Elevated cerebrospinal fluid tau in Wernicke encephalopathy

Tau as a Biomarker of Neurodegenerative Diseases

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