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Tau Protein Levels (tau + protein_level)

Distribution by Scientific Domains

Life Sciences	60%

Selected Abstracts

Elevated Cerebrospinal Fluid Tau Protein Levels in Wernicke's Encephalopathy

ALCOHOLISM, Issue 6 2008
Sachio Matsushita
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 ,-protein ending at amino acid 42 (A,42) 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 A,42 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. [source]

Truncated tau expression levels determine life span of a rat model of tauopathy without causing neuronal loss or correlating with terminal neurofibrillary tangle load

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2008
Peter Koson
Abstract We have previously demonstrated in a transgenic rat model of tauopathy that human misfolded truncated tau derived from Alzheimer's disease suffices to drive neurofibrillary degeneration in vivo. We employed this model to investigate the impact of truncated tau expression levels on life span, neuronal loss and the final load of neurofibrillary tangles (NFTs) in transgenic rats. Two independent transgenic lines (SHR72, SHR318), that display different expression levels of truncated tau, were utilized in this study. We found that transgene expression levels in the brain of SHR72 rats were 44% higher than in SHR318 rats and that truncated tau protein levels determined the survival rate of transgenic rats. The line with higher expression levels of truncated tau (SHR72) showed decreased median survival (222.5 days) when compared with the line with lower expression (SHR318; 294.5 days). Interestingly, NFT loads (total NFT/total neurons) were very similar in terminal stages of disease in both transgenic lines (SHR72 , 10.9%; SHR318 , 11.6%), despite significantly different expression levels of truncated tau. Moreover, mean neuron numbers in the hippocampus (CA1,3) and brain stem (gigantocellular reticular nucleus) in the two transgenic rat strains in the terminal stages of disease were similar, and did not differ significantly from those observed in age-matched non-transgenic controls. These findings suggest that the expression levels of misfolded truncated tau determine the life span in a transgenic rat model of tauopathy without causing neuronal loss or correlating with terminal NFT load. [source]

Oxidative stress increases levels of endogenous amyloid-, peptides secreted from primary chick brain neurons

AGING CELL, Issue 5 2008
Claire Goldsbury
Summary Oxidative damage is associated with Alzheimer's disease and mild cognitive impairment, but its relationship to the development of neuropathological lesions involving accumulation of amyloid-, (A,) peptides and hyperphosphorylated tau protein remains poorly understood. We show that inducing oxidative stress in primary chick brain neurons by exposure to sublethal doses of H2O2 increases levels of total secreted endogenous A, by 2.4-fold after 20 h. This occurs in the absence of changes to intracellular amyloid precursor protein or tau protein levels, while heat-shock protein 90 is elevated 2.5-fold. These results are consistent with the hypothesis that aging-associated oxidative stress contributes to increasing A, generation and up-regulation of molecular chaperones in Alzheimer's disease. [source]

Antisense suppression of tau in cultured rat oligodendrocytes inhibits process formation

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 12 2008
David Gordon
Abstract The microtubule-associated protein tau is integral to neuronal process development and has a role in the pathogenesis of several neurodegenerative conditions. We examined possible roles for tau in cultured oligodendrocyte process formation by using antisense oligonucleotide treatment. Inhibition of tau synthesis with single oligonucleotides resulted in decreased tau protein levels and significantly shorter cellular processes. Simultaneous use of two nonoverlapping oligonucleotides caused a major reduction in tau levels and severely inhibited process outgrowth. The timing of oligonucleotide addition to oligodendrocyte cultures was important, with addition of antisense at the time of plating into culture having the most significant effect on morphology through reduction of tau expression. © 2008 Wiley-Liss, Inc. [source]