Total Tau (total + tau)

Distribution by Scientific Domains


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]


Cerebrospinal fluid biomarkers of white matter lesions , cross-sectional results from the LADIS study

EUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2010
M. Jonsson
Background and purpose:, White matter lesions (WMLs) caused by small vessel disease are common in elderly people and contribute to cognitive impairment. There are no established biochemical markers for WMLs. We aimed to study the relation between degree of WMLs rated on magnetic resonance imaging of the brain and cerebrospinal fluid (CSF) levels of structural biomarkers associated with Alzheimer's disease (AD) and subcortical vascular dementia. Methods:, Fifty-three non-demented elderly individuals with WMLs were subjected to lumbar puncture. Degree of WMLs was rated using the Fazekas scale. Volumetric assessment of WMLs was performed. CSF samples were analyzed for the 40 and 42 amino acid fragments of amyloid ,, ,- and ,-cleaved soluble amyloid precursor protein, total tau (T-tau), hyperphosphorylated tau (P-tau181), neurofilament light protein (NFL), sulfatide and CSF/Serum-albumin ratio. Results:, Fifteen subjects had mild, 23 had moderate and 15 had severe degree of WMLs. CSF-NFL levels differed between the groups (P < 0.001) and correlated with the volume of WMLs (r = 0.477, P < 0.001). CSF sulfatide concentration displayed similar changes but less strongly. T-tau, P-tau181 and the different amyloid markers as well as CSF/S-albumin ratio did not differ significantly between the groups. Conclusions:, The association of increased CSF-NFL levels with increasing severity of WMLs in non-demented subjects suggests that NFL is a marker for axonal damage in response to small vessel disease in the brain. This manifestation may be distinct from or earlier than the neurodegenerative process seen in AD, as reflected by the lack of association between WMLs and AD biomarkers. [source]


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]


Cerebrospinal fluid amyloid ,40 is decreased in cerebral amyloid angiopathy,

ANNALS OF NEUROLOGY, Issue 2 2009
Marcel M. Verbeek MSc
Cerebral amyloid angiopathy is caused by deposition of the amyloid , protein in the cerebral vasculature. In analogy to previous observations in Alzheimer disease, we hypothesized that analysis of amyloid ,40 and ,42 proteins in the cerebrospinal fluid might serve as a molecular biomarker. We observed strongly decreased cerebrospinal fluid amyloid ,40 (p < 0.01 vs controls or Alzheimer disease) and amyloid ,42 concentrations (p < 0.001 vs controls and p < 0.05 vs Alzheimer disease) in cerebral amyloid angiopathy patients. The combination of amyloid ,42 and total tau discriminated cerebral amyloid angiopathy from controls, with an area under the receiver operator curve of 0.98. Our data are consistent with neuropathological evidence that amyloid ,40 as well as amyloid ,42 protein are selectively trapped in the cerebral vasculature from interstitial fluid drainage pathways that otherwise transport amyloid , proteins toward the cerebrospinal fluid. Ann Neurol 2009;66:245,249 [source]


Cerebrospinal fluid biomarker signature in Alzheimer's disease neuroimaging initiative subjects,

ANNALS OF NEUROLOGY, Issue 4 2009
Leslie M. Shaw PhD
Objective Develop a cerebrospinal fluid biomarker signature for mild Alzheimer's disease (AD) in Alzheimer's Disease Neuroimaging Initiative (ADNI) subjects. Methods Amyloid-, 1 to 42 peptide (A,1,42), total tau (t-tau), and tau phosphorylated at the threonine 181 were measured in (1) cerebrospinal fluid (CSF) samples obtained during baseline evaluation of 100 mild AD, 196 mild cognitive impairment, and 114 elderly cognitively normal (NC) subjects in ADNI; and (2) independent 56 autopsy-confirmed AD cases and 52 age-matched elderly NCs using a multiplex immunoassay. Detection of an AD CSF profile for t-tau and A,1,42 in ADNI subjects was achieved using receiver operating characteristic cut points and logistic regression models derived from the autopsy-confirmed CSF data. Results CSF A,1,42 was the most sensitive biomarker for AD in the autopsy cohort of CSF samples: receiver operating characteristic area under the curve of 0.913 and sensitivity for AD detection of 96.4%. In the ADNI cohort, a logistic regression model for A,1,42, t-tau, and APO,4 allele count provided the best assessment delineation of mild AD. An AD-like baseline CSF profile for t-tau/A,1,42 was detected in 33 of 37 ADNI mild cognitive impairment subjects who converted to probable AD during the first year of the study. Interpretation The CSF biomarker signature of AD defined by A,1,42 and t-tau in the autopsy-confirmed AD cohort and confirmed in the cohort followed in ADNI for 12 months detects mild AD in a large, multisite, prospective clinical investigation, and this signature appears to predict conversion from mild cognitive impairment to AD. Ann Neurol 2009 [source]


Tau haplotype influences cerebral perfusion pattern in frontotemporal lobar degeneration and related disorders

ACTA NEUROLOGICA SCANDINAVICA, Issue 5 2008
B. Borroni
Objective,,, The modulating factors on phenotypic expression of frontotemporal lobar degeneration (FTLD) remain still unknown. The aim of this study was to determine whether tau genetic variability modulates the brain functional and the clinical phenotypic expression of FTLD. Materials and methods,,, Clinical and neurological evaluations, a standardized neuropsychological assessments as well as a brain single photon emission tomography perfusion imaging studies were performed in 48 FTLD patients. Cerebral perfusion patterns were analysed according to H1 or H2 tau haplotypes by statistical parametric mapping and principal component analysis. Results,,, Two different patterns of cerebral dysfunction characterized the haplotypes, as hypoperfusion of frontal medial and cingulated cortex in H2-carriers and a prevalent involvement of posterior parietal regions in H1-carriers. Further, a significant increase of cerebrospinal fluid total tau and phospho tau levels was found in H2-carriers. Conclusions,,, These findings support a role of tau haplotype in modulating disease phenotype by influencing the hypoperfusion pattern and cerebrospinal fluid tau levels in FTLD. [source]