&lt;i&gt;Tau&lt;/i&gt; Immunoreactivity Detected in Human Plasma, But No Obvious Increase in Dementia

Ingelson, Martin; Blomberg, Mari; Benedikz, Eiríkur; Wahlund, Lars‐Olof; Karlsson, Evert; Vanmechelen, Eugeen; Lannfelt, Lars

doi:10.1159/000017187

Cited by 32 publications

(23 citation statements)

References 21 publications

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“…It is possible that tau entering serum compartments is enzymatically cleaved, loses its C-terminal part, and consequently the first step of t-tau assay becomes unfeasible even though p-tau is still efficiently detected. On the other hand, in a previously published study [31], serum tau immunoreactivity detection in patients with dementia was approximately 20% (similar to our results) but after gel filtration peak reactivity was found in the 160kD fraction. This indicated an unexpected high molecular weight, and suggested the existence of tau-like molecules or polymers of lowmolecular weight tau.…”

Section: Figure 1 Linear Regression Line With 95% CI Band For Csf Tasupporting

confidence: 92%

CSF and serum total-tau and phospho-tau(181P) in MS patients

2011

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AbstractIn search of biological marker in multiple sclerosis (MS), total-tau and phospho-tau (Thr181) concentrations were established in CSF and serum of 78 patients with MS, using commercially available kits. Serum and CSF concentrations of IgG, IgM, and albumin were assayed simultaneously to calculate quotients and indices of intrathecal synthesis. Serum t-tau detection was strikingly low (23.1%); therefore, this factor was excluded from further analysis. Serum p-tau levels did not correlate with any of indices or quotients. Unexpectedly, CSF t-tau and p-tau showed an inverse relation with MSSS and EDSS, which has not been published elsewhere. Our results do not support utility of serum t-tau and p-tau as surrogate markers for MS.

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Section: Figure 1 Linear Regression Line With 95% CI Band For Csf Tasupporting

confidence: 92%

CSF and serum total-tau and phospho-tau(181P) in MS patients

2011

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“…They are generally expensive to perform routinely and lumbar puncture is invasive and often unpleasant. Moreover a large variability exists in the literature as to CSF biomarker diagnostic accuracies and cut-offs, hampering or delaying their everyday application in the clinical setting [29, 30] and their potential use as indicators of prodromal AD.…”

Section: Biomarkersmentioning

confidence: 99%

Peripheral Blood Mononuclear Cells as a Laboratory to Study Dementia in the Elderly

Arosio

D’Addario

Gussago

et al. 2014

BioMed Research International

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The steady and dramatic increase in the incidence of Alzheimer's disease (AD) and the lack of effective treatments have stimulated the search for strategies to prevent or delay its onset and/or progression. Since the diagnosis of dementia requires a number of established features that are present when the disease is fully developed, but not always in the early stages, the need for a biological marker has proven to be urgent, in terms of both diagnosis and monitoring of AD. AD has been shown to affect peripheral blood mononuclear cells (PBMCs) that are a critical component of the immune system which provide defence against infection. Although studies are continuously supplying additional data that emphasize the central role of inflammation in AD, PBMCs have not been sufficiently investigated in this context. Delineating biochemical alterations in AD blood constituents may prove valuable in identifying accessible footprints that reflect degenerative processes within the Central Nervous System (CNS). In this review, we address the role of biomarkers in AD with a focus on the notion that PBMCs may serve as a peripheral laboratory to find molecular signatures that could aid in differential diagnosis with other forms of dementia and in monitoring of disease progression.

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“…The interassay variation is between 1.7 and 6% [13]. The probe volume was increased to 75 µl and the conjugate decreased to 25 µl to lower the detection limit for serum samples [10]. …”

Section: Methodsmentioning

confidence: 99%

“…So far, there is limited experience with serum levels of tau protein. In one study, no differences of plasma tau protein levels were found between patients with dementia and controls [10]. …”

Section: Introductionmentioning

confidence: 99%

Serum Tau Protein Level as a Marker of Axonal Damage in Acute Ischemic Stroke

et al. 2002

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Biochemical markers of brain damage, e.g. ischemic stroke, should reflect the volume of irreversibly damaged brain parenchyma and the clinical outcome in a single patient in order to allow estimation of prognosis at an early stage. Tau protein, which derives predominantly from neurons and axons, is elevated in the cerebrospinal fluid of patients with neurodegenerative disease. This makes tau protein a potential marker of neuronal/axonal injury. In order to test this hypothesis, the current study aimed at showing that tau protein is measurable in the blood after acute ischemic stroke and that it correlates with clinical disability and stroke volume. In a longitudinal prospective study we measured tau protein serum levels with an ELISA in 30 patients longitudinally after ischemic stroke. Tau protein was detectable within 5 days after ischemia in the sera of 7/20 patients with MRI-proven infarction and in 2/10 patients with transitory ischemic attack; both of them had a small infarction visible on the MRI scan. Tau protein was measurable within 6 h after symptom onset, peaked after 3–5 days and correlated with infarct volume and disability after 3 months. In conclusion, serum tau protein is a candidate marker of axonal injury. In stroke, its clinical use is limited, because it is detectable only in a proportion of patients.

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<i>Tau</i> Immunoreactivity Detected in Human Plasma, But No Obvious Increase in Dementia

Cited by 32 publications

References 21 publications

CSF and serum total-tau and phospho-tau(181P) in MS patients

CSF and serum total-tau and phospho-tau(181P) in MS patients

Peripheral Blood Mononuclear Cells as a Laboratory to Study Dementia in the Elderly

Serum Tau Protein Level as a Marker of Axonal Damage in Acute Ischemic Stroke

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