Phosphorylated Tau 181 (pTau-181), Plasma

CPT: 83520

Special Instructions

This assay is currently not available in New York state.

This test may exhibit interference when sample is collected from a person who is consuming a supplement with a high dose of biotin (also termed as vitamin B7 or B8, vitamin H, or coenzyme R). It is recommended to ask all patients who may be indicated for this test about biotin supplementation. Patients should be cautioned to stop biotin consumption at least 72 hours prior to the collection of a sample.

Expected Turnaround Time

1 - 3 days

Related Documents

Specimen Requirements


EDTA plasma


1 mL

Minimum Volume

0.7 mL (Note: This volume does not allow for repeat testing.)


Lavender-top (EDTA) tube


Draw blood in lavender-top (EDTA) tube. Invert to mix with preservatives. Centrifuge and transfer plasma to a labeled plastic transport tube.

Storage Instructions

Room temperature

Stability Requirements



Room temperature

14 days


14 days


14 days

Freeze/thaw cycles

Stable x3

Causes for Rejection

Serum specimen; improper labeling

Test Details


This test is used for the measurement of the level of Phosphorylated Tau 181 (pTau-181) in plasma.


This test was developed and its performance characteristics determined by Labcorp. It has not been cleared or approved by the Food and Drug Administration.

This test is performed by Roche Diagnostics Electrochemiluminescence Immunoassay (ECLIA). Values obtained with different assay methods or kits cannot be used interchangeably.

Hepatic and renal function impact concentrations of pTau-181.1,2

Results of plasma pTau-181 testing in patients with a history of myocardial infarction (MI) or clinical stroke should be interpreted with caution.2


Roche Diagnostics Electrochemiluminescence Immunoassay (ECLIA)

Reference Interval

0.00–0.95 pg/mL (reference interval is based on a population of ostensibly healthy individuals aged 20 to 55 years)

Additional Information

Definitive diagnosis of Alzheimer disease (AD) is established by autopsy confirmation of two major pathological hallmarks: extracellular amyloid plaques consisting of aggregated amyloid-β (Aβ) peptides, and intracellular neurofibrillary tangles containing abnormally phosphorylated tau (pTau).3 Up to a third of living individuals diagnosed with AD exclusively on the basis of clinical symptoms do not have AD neuropathological changes post-mortem.4 A biological definition of AD was recently proposed by the National Institute on Aging and the Alzheimer's Association (NIA-AA).5 According the AT(N) system that they proposed, AD is biologically defined by biomarker evidence determined by either CSF biomarker concentrations or via Positron Emission Tomography (PET) of Aβ or tau, regardless of the accompanying clinical syndrome.5 In this framework, neurodegeneration (N) is defined by MRI-based identification of hippocampal atrophy or glucose hypometabolism (fluorodeoxyglucose PET), elevation of CSF total tau or elevation of CSF NfL.5 In living individuals, AD-related pathophysiological changes can be accurately detected with PET imaging of the intensity and distribution of Aβ plaques and tau neurofibrillary tangles, structural MRI of brain atrophy,6 and/or the evaluation of alterations in CSF levels of Aβ1–42 (or the Aβ1–42 to Aβ1–40 ratio), phosphorylated tau (pTau) and total tau (or neurofilament light (NfL).7-9 These established biomarkers are predictive of autopsy findings,10,11 and are thus included in research and clinical criteria for the definition and staging of AD.5,12-14

The mid-region of tau protein has several threonine and serine residues that can be phosphorylation by specific kinases.15-18 This phosphorylation can occur at numerous locations, including amino acids 181, 199, 202, 205, 217, 231, 235 and 396. pTau has known physiological functions, including maintenance of microtubule assembly and stability.19 However, excessive phosphorylation has pathophysiological consequences.20,21 In patients with AD, some fractions of the phosphorylated tau pool in the brain progressively aggregate into insoluble filamentous deposits that can be detected in neuropathology and PET investigations.16,22 Concomitantly, some soluble pTau fractions accumulate in the CSF, where they can be detected and quantified to provide indirect evidence of disease state.9,23-27 The accumulation of pTau in the CSF seems to be specifically induced by Aβ pathology (plaques) and does not occur to a significant extent in individuals with Aβ-negative non-AD tauopathies.28 As a consequence, CSF pTau is used as an indirect marker of AD-type brain tau pathology and increases with disease progression and is associated with incremental neurofibrillary tangle formation.28-32 A fraction of the pTau protein in the CSF diffuses into the blood where it too can be measured in the assessment of AD status.28,33

The clinical application of plasma p-tau biomarkers in AD has been reviewed extensively.34-38 The measurement of plasma of pTau phosphorylated and amino acid 181 (pTau-181) for the assessment of AD clinical status has been investigated in numerous clinical settings.15,25,37,39-67 Plasma pTau-181 concentrations have been shown to correlate with tau PET in patients suspected of having AD.49,55,62,64,68 Plasma pTau-181 levels have been shown to be higher in Aβ-positive, tau-negative individuals than in Aβ-negative, tau negative individuals.15,55 pTau-181 levels are generally higher in patients with preclinical AD (i.e., early stage disease where individuals do not have overt symptoms but are positive for CSF or PET biomarkers; these individuals are often Aβ-positive but tau-negative) than in patients otherwise healthy individuals.15,25,41,42,53,57,65,68 A relative elevation of pTau-181 has also been observed in patients with prodromal AD (i.e., individuals with mild cognitive impairment who are positive for CSF or PET biomarkers).2,15,41,54,57 Evidence from multiple studies has shown that plasma pTau-181 levels increase as patients with AD progress to dementia.49,55-57,60-62,64,68 Other studies have found that plasma pTau-181 concentration differentiated individuals with autopsy-verified AD dementia from Aβ-negative control participants.15,37,44,52,69 In familial AD, plasma levels of pTau-181 were higher in symptomatic mutation carriers than in cognitively healthy non-carriers.57 Plasma pTau-181 accurately differentiated individuals with Down syndrome dementia from individuals with Down syndrome and no dementia and age-matched control participants.54,67 A number of studies have found that plasma pTau-181 concentrations increase with AD disease progression and worsening of cognition, brain Aβ burden, brain tau burden and brain atrophy.7,15,40,41,44,51,55-58,62,68,70-72

Numerous studies have reported that measurement of plasma pTau-181 can predict the extent of brain amyloid and tau as measured by PET.9,15,29,39-62 In general, these studies have included patients with limited clinical pathologies other than those associated with AD. As a consequence, it has been suggested that the results of these studies may not be completely generalizable to the population as a whole.2 In a recent study, Mielke and coworkers2 evaluated factors that could affect the interpretation of the plasma pTau-181 at the population level. Their study of the concentration of plasma pTau-181 in a community-based cohort allowed them to discern the effect of coexisting comorbidities on the measured concentrations of plasma pTau-181. Consistent with previously published studies,49 Mielke found that plasma pTau-181 increased with age starting between the ages of 65 and 70 years. However, they found that this increase was most pronounced among those with elevated brain amyloid. A diagnosis of chronic kidney disease (CKD) or a history of myocardial infarction (MI) or clinical stroke also had an effect on the population distribution of plasma pTau-181 concentrations.2 By testing a reference population consisting of amyloid negative individuals with no history of CKD, MI or stroke, Mielke went on to define a single, fixed clinical threshold for plasma pTau-181 for all ages.2 Using this single threshold, they reported that plasma pTau-181 proved to be an excellent predictor of elevated brain amyloid and tau PET in the entorhinal cortex.2 Based on this finding, Labcorp has defined a single clinical threshold for pTau-181 using a ostensibly normal, chemically screened population of individuals between 20 and 55 years of age. This clinical threshold is applied as a “reference Interval” for all patient reports.


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