Phosphorylated Tau 181 (pTau-181), Plasma

CPT: 83520
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Special Instructions

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


Specimen

EDTA plasma


Volume

1 mL


Minimum Volume

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


Container

Lavender-top (EDTA) tube


Collection

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

Temperature

Period

Room temperature

14 days

Refrigerated

14 days

Frozen

14 days

Freeze/thaw cycles

Stable x3


Causes for Rejection

Serum specimen; improper labeling


Test Details


Use

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


Limitations

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


Methodology

Roche Diagnostics Electrochemiluminescence Immunoassay (ECLIA)


Reference Interval

• 0 - 55 years: 0.00–0.95 pg/mL

Reference interval is based on a population of ostensibly healthy individuals aged 20 to 55 years. Test performed by Roche Diagnostics Electrochemiluminescence Immunoassay (ECLIA). Values obtained with different methods cannot be used interchangeable.

• >55 years: 0.00–0.97 pg/mL

Results greater than the clinical cut-off of 0.97 pg/mL in patients greater than 55 years of age are correlated with Abeta amyloid pathology as determined by amyloid PET imaging. Test performed by Roche Diagnostics Electrochemiluminescence Immunoassay (ECLIA). Values obtained with different methods cannot be used interchangeable.


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.


Footnotes

1. Berry K, Asken BM, Grab JD, et al. Hepatic and renal function impact concentrations of plasma biomarkers of neuropathology. Alzheimers Dement (Amst). 2022 Jul 12;14(1):e12321.35845260
2. Mielke MM, Dage JL, Frank RD, et al. Performance of plasma phosphorylated tau 181 and 217 in the community. Nat Med. 2022 Jul;28(7):1398-1405.35618838
3. DeTure MA, Dickson DW. The neuropathological diagnosis of Alzheimer's disease. Mol Neurodegener. 2019 Aug 2;14(1):32.31375134
4. Beach TG, Monsell SE, Phillips LE, Kukull W. Accuracy of the clinical diagnosis of Alzheimer disease at National Institute on Aging Alzheimer Disease Centers, 2005-2010. J Neuropathol Exp Neurol. 2012 Apr;71(4):266-273.22437338
5. Jack CR Jr, Bennett DA, Blennow K, et al. NIA-AA Research Framework: Toward a biological definition of Alzheimer's disease. Alzheimers Dement. 2018 Apr;14(4):535-562.29653606
6. Nordberg A, Rinne JO, Kadir A, Långström B. The use of PET in Alzheimer disease. Nat Rev Neurol. 2010 Feb;6(2):78-87.20139997
7. Ashton NJ, Hye A, Rajkumar AP, Leuzy A, et al. An update on blood-based biomarkers for non-Alzheimer neurodegenerative disorders. Nat Rev Neurol. 2020 May;16(5):265-284.32322100
8. Blennow K, Hampel H, Weiner M, Zetterberg H. Cerebrospinal fluid and plasma biomarkers in Alzheimer disease. Nat Rev Neurol. 2010 Mar;6(3):131-144.20157306
9. Leuzy A, Ashton NJ, Mattsson-Carlgren N, et al. 2020 update on the clinical validity of cerebrospinal fluid amyloid, tau, and phospho-tau as biomarkers for Alzheimer's disease in the context of a structured 5-phase development framework. Eur J Nucl Med Mol Imaging. 2021 Jul;48(7):2121-2139.33674895
10. Seeburger JL, Holder DJ, Combrinck M, et al. Cerebrospinal fluid biomarkers distinguish postmortem-confirmed Alzheimer's disease from other dementias and healthy controls in the OPTIMA cohort. J Alzheimers Dis. 2015;44(2):525-539.25391385
11. Engelborghs S, De Vreese K, Van de Casteele T, et al. Diagnostic performance of a CSF-biomarker panel in autopsy-confirmed dementia. Neurobiol Aging. 2008 Aug;29(8):1143-1159.17428581
12. Dubois B, Villain N, Frisoni GB, et al. Clinical diagnosis of Alzheimer's disease: recommendations of the International Working Group. Lancet Neurol. 2021 Jun;20(6):484-496.33933186
13. Fleisher AS, Pontecorvo MJ, Devous MD Sr, et al. A16 Study Investigators. Positron Emission Tomography Imaging With [18F]flortaucipir and Postmortem Assessment of Alzheimer Disease Neuropathologic Changes. JAMA Neurol. 2020 Jul 1;77(7):829-839.32338734
14. Dubois B, Feldman HH, Jacova C, et al. Advancing research diagnostic criteria for Alzheimer's disease: the IWG-2 criteria. Lancet Neurol. 2014;13(6):614-629.24849862
15. Lantero Rodriguez J, Karikari TK, et al. Plasma p-tau181 accurately predicts Alzheimer's disease pathology at least 8 years prior to post-mortem and improves the clinical characterisation of cognitive decline. Acta Neuropathol. 2020 Sep;140(3):267-278.32720099
16. Barthélemy NR, Li Y, Joseph-Mathurin N, Gordon BA, et al. Dominantly Inherited Alzheimer Network. A soluble phosphorylated tau signature links tau, amyloid and the evolution of stages of dominantly inherited Alzheimer's disease. Nat Med. 2020 Mar;26(3):398-407.32161412
17. Hanger DP, Byers HL, Wray S, et al. Novel phosphorylation sites in tau from Alzheimer brain support a role for casein kinase 1 in disease pathogenesis. J Biol Chem. 2007 Aug 10;282(32):23645-23654.17562708
18. Hanger DP, Betts JC, Loviny TL, Blackstock WP, Anderton BH. New phosphorylation sites identified in hyperphosphorylated tau (paired helical filament-tau) from Alzheimer's disease brain using nanoelectrospray mass spectrometry. J Neurochem. 1998 Dec;71(6):2465-2476.983214
19. Hill E, Wall MJ, Moffat KG, Karikari TK. Understanding the Pathophysiological Actions of Tau Oligomers: A Critical Review of Current Electrophysiological Approaches. Front Mol Neurosci. 2020 Aug 20;13:155.32973448
20. Hanger DP, Anderton BH, Noble W. Tau phosphorylation: the therapeutic challenge for neurodegenerative disease. Trends Mol Med. 2009 Mar;15(3):112-119.19246243
21. Augustinack JC, Schneider A, Mandelkow EM, Hyman BT. Specific tau phosphorylation sites correlate with severity of neuronal cytopathology in Alzheimer's disease. Acta Neuropathol. 2002 Jan;103(1):26-35.11837744
22. Braak H, Braak E. Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol. 1991;82(4):239-259.1759558
23. Karikari TK, Emeršič A, Vrillon A, et al. Head-to-head comparison of clinical performance of CSF phospho-tau T181 and T217 biomarkers for Alzheimer's disease diagnosis. Alzheimers Dement. 2021 May;17(5):755-767.33252199
24. Hanes J, Kovac A, Kvartsberg H, et al. Evaluation of a novel immunoassay to detect p-tau Thr217 in the CSF to distinguish Alzheimer disease from other dementias. Neurology. 2020 Dec 1;95(22):e3026-e3035.32973122
25. Suárez-Calvet M, Karikari TK, Ashton NJ, et al. ALFA Study. Novel tau biomarkers phosphorylated at T181, T217 or T231 rise in the initial stages of the preclinical Alzheimer's continuum when only subtle changes in Aβ pathology are detected. EMBO Mol Med. 2020 Dec 7;12(12):e12921.33169916
26. Koss DJ, Jones G, Cranston A, Gardner H, Kanaan NM, Platt B. Soluble pre-fibrillar tau and β-amyloid species emerge in early human Alzheimer's disease and track disease progression and cognitive decline. Acta Neuropathol. 2016 Dec;132(6):875-895.27770234
27. Buerger K, Teipel SJ, Zinkowski R, et al. CSF tau protein phosphorylated at threonine 231 correlates with cognitive decline in MCI subjects. Neurology. 2002 Aug 27;59(4):627-629.12196665
28. Sato C, Barthélemy NR, Mawuenyega KG, et al. Tau Kinetics in Neurons and the Human Central Nervous System. Neuron. 2018 May 16;98(4):861-864.29772204
29. Krell-Roesch J, Rakusa M, Syrjanen JA, et al. Association between CSF biomarkers of Alzheimer's disease and neuropsychiatric symptoms: Mayo Clinic Study of Aging. Alzheimers Dement. 2022 Feb 9.35142047
30. Paraskevas GP. The Role of Cerebrospinal Fluid Biomarkers in Dementia and Other Related Neurodegenerative Disorders. Brain Sci. 2022 May 11;12(5):627.35625013
31. Hansson O, Zetterberg H, Buchhave P, Londos E, Blennow K, Minthon L. Association between CSF biomarkers and incipient Alzheimer's disease in patients with mild cognitive impairment: a follow-up study. Lancet Neurol. 2006 Mar;5(3):228-234.16488378
32. Mattsson N, Schöll M, Strandberg O, et al. 18F-AV-1451 and CSF T-tau and P-tau as biomarkers in Alzheimer's disease. EMBO Mol Med. 2017 Sep;9(9):1212-1223.28743782
33. Han P, Serrano G, Beach TG, et al. A Quantitative Analysis of Brain Soluble Tau and the Tau Secretion Factor. J Neuropathol Exp Neurol. 2017 Jan 1;76(1):44-51.28069930
34. Karikari TK, Ashton NJ, Brinkmalm G, et al. Blood phospho-tau in Alzheimer disease: analysis, interpretation, and clinical utility. Nat Rev Neurol. 2022 Jul;18(7):400-418.35585226
35. Park SA, Jang YJ, Kim MK, Lee SM, Moon SY. Promising Blood Biomarkers for Clinical Use in Alzheimer's Disease: A Focused Update. J Clin Neurol. 2022 Jul;18(4):401-409.35796265
36. Mankhong S, Kim S, Lee S, et al. Development of Alzheimer's Disease Biomarkers: From CSF- to Blood-Based Biomarkers. Biomedicines. 2022 Apr 5;10(4):850.35453600
37. Ashton NJ, Leuzy A, Karikari TK, et al. The validation status of blood biomarkers of amyloid and phospho-tau assessed with the 5-phase development framework for AD biomarkers. Eur J Nucl Med Mol Imaging. 2021 Jul;48(7):2140-2156.33677733
38. Barro C, Zetterberg H. The blood biomarkers puzzle - A review of protein biomarkers in neurodegenerative diseases. J Neurosci Methods. 2021 Sep 1;361:109281.34237384
39. Brickman AM, Manly JJ, Honig LS, et al. Correlation of plasma and neuroimaging biomarkers in Alzheimer's disease. Ann Clin Transl Neurol. 2022 May;9(5):756-761.35306760
40. Chatterjee P, Pedrini S, Ashton NJ, et al. Diagnostic and prognostic plasma biomarkers for preclinical Alzheimer's disease. Alzheimers Dement. 2022 Jun;18(6):1141-1154.34494715
41. De Meyer S, Vanbrabant J, Schaeverbeke JM, et al. Phospho-specific plasma p-tau181 assay detects clinical as well as asymptomatic Alzheimer's disease. Ann Clin Transl Neurol. 2022 May;9(5):734-746.35502634
42. McGrath ER, Beiser AS, O'Donnell A, et al. Blood Phosphorylated Tau 181 as a Biomarker for Amyloid Burden on Brain PET in Cognitively Healthy Adults. J Alzheimers Dis. 2022;87(4):1517-1526.3549178
43. Meyer PF, Ashton NJ, Karikari TK, et al. Presymptomatic Evaluation of Experimental or Novel Treatments for Alzheimer Disease (PREVENT-AD) Research Group. Plasma p-tau231, p-tau181, PET Biomarkers, and Cognitive Change in Older Adults. Ann Neurol. 2022 Apr;91(4):548-560.35084051
44. Smirnov DS, Ashton NJ, Blennow K, et al. Plasma biomarkers for Alzheimer's Disease in relation to neuropathology and cognitive change. Acta Neuropathol. 2022 Apr;143(4):487-503.35195758
45. Thijssen EH, Verberk IMW, Kindermans J, et al. Differential diagnostic performance of a panel of plasma biomarkers for different types of dementia. Alzheimers Dement (Amst). 2022 May 15;14(1):e12285.35603139
46. Tsiknia AA, Edland SD, Sundermann EE, et al. Sex differences in plasma p-tau181 associations with Alzheimer's disease biomarkers, cognitive decline, and clinical progression. Mol Psychiatry. 2022 Oct;27(10):4314-4322. Epub 2022 Jun 29.35768637
47. Alcolea D, Delaby C, Muñoz L, et al. Use of plasma biomarkers for AT(N) classification of neurodegenerative dementias. J Neurol Neurosurg Psychiatry. 2021 Nov;92(11):1206-1214.34103344
48. Bayoumy S, Verberk IMW, den Dulk B, et al. Clinical and analytical comparison of six Simoa assays for plasma P-tau isoforms P-tau181, P-tau217, and P-tau231. Alzheimers Res Ther. 2021 Dec 4;13(1):198.34863295
49. Brickman AM, Manly JJ, Honig LS, et al. Plasma p-tau181, p-tau217, and other blood-based Alzheimer's disease biomarkers in a multi-ethnic, community study. Alzheimers Dement. 2021 Aug;17(8):1353-1364.33580742
50. Chong JR, Ashton NJ, Karikari TK, et al. Plasma P-tau181 to Aβ42 ratio is associated with brain amyloid burden and hippocampal atrophy in an Asian cohort of Alzheimer's disease patients with concomitant cerebrovascular disease. Alzheimers Dement. 2021 Oct;17(10):1649-1662.33792168
51. Clark C, Lewczuk P, Kornhuber J, et al. Plasma neurofilament light and phosphorylated tau 181 as biomarkers of Alzheimer's disease pathology and clinical disease progression. Alzheimers Res Ther. 2021 mar 25;13(1):65.33766131
52. Grothe MJ, Moscoso A, Ashton NJ, et al. Associations of Fully Automated CSF and Novel Plasma Biomarkers With Alzheimer Disease Neuropathology at Autopsy. Neurology. 2021 Jul 15;97(12):e1229-1242.34266917
53. Keshavan A, Pannee J, Karikari TK, et al. Population-based blood screening for preclinical Alzheimer's disease in a British birth cohort at age 70. Brain. 2021 Mar 3;144(2):434-449.33479777
54. Lleó A, Zetterberg H, Pegueroles J, et al. Phosphorylated tau181 in plasma as a potential biomarker for Alzheimer's disease in adults with Down syndrome. Nat Commun. 2021 Jul 14;12(1):4304.34262030
55. Moscoso A, Grothe MJ, Ashton NJ, et al. Time course of phosphorylated-tau181 in blood across the Alzheimer's disease spectrum. Brain. 2021 Feb 12;144(1):325-339.33257949
56. Moscoso A, Grothe MJ, Ashton, et al. Longitudinal Associations of Blood Phosphorylated Tau181 and Neurofilament Light Chain With Neurodegeneration in Alzheimer Disease. JAMA Neurol. 2021 Apr 1;78(4):396-406.33427873
57. O'Connor A, Karikari TK, Poole T, et al. Plasma phospho-tau181 in presymptomatic and symptomatic familial Alzheimer's disease: a longitudinal cohort study. Mol Psychiatry. 2021 Oct;26(10):5967-5976.32665603
58. Simrén J, Ashton NJ, Blennow K, Zetterberg H. Blood neurofilament light in remote settings: Alternative protocols to support sample collection in challenging pre-analytical conditions. Alzheimers Dement (Amst). 2021 Feb 20;13(1):e12145.33665338
59. Thijssen EH, La Joie R, Strom A, et al. Advancing Research and Treatment for Frontotemporal Lobar Degeneration investigators. Plasma phosphorylated tau 217 and phosphorylated tau 181 as biomarkers in Alzheimer's disease and frontotemporal lobar degeneration: a retrospective diagnostic performance study. Lancet Neurol. 2021 Sep;20(9):739-752.34418401
60. Zettergren A, Lord J, Ashton NJ, et al; Alzheimer’s Disease Neuroimaging Initiative. Association between polygenic risk score of Alzheimer's disease and plasma phosphorylated tau in individuals from the Alzheimer's Disease Neuroimaging Initiative. Alzheimers Res Ther. 2021 Jan 8;13(1):17.33419453
61. Benussi A, Karikari TK, Ashton N, et al. Diagnostic and prognostic value of serum NfL and p-Tau181 in frontotemporal lobar degeneration. J Neurol Neurosurg Psychiatry. 2020 Sep;91(9):960-967.32611664
62. Karikari TK, Pascoal TA, Ashton N, et al. Blood phosphorylated tau 181 as a biomarker for Alzheimer's disease: a diagnostic performance and prediction modelling study using data from four prospective cohorts. Lancet Neurol. 2020 May;19(5):422-433.32333900
63. Shen XN, Li JQ, Wang HF, et al; Alzheimer's Disease Neuroimaging Initiative. Plasma amyloid, tau, and neurodegeneration biomarker profiles predict Alzheimer's disease pathology and clinical progression in older adults without dementia. Alzheimers Dement (Amst). 2020 Sep 24;12(1):e12104.33005724
64. Thijssen EH, La Joie R, Wolf A, et al. Advancing Research and Treatment for Frontotemporal Lobar Degeneration (ARTFL) investigators. Diagnostic value of plasma phosphorylated tau181 in Alzheimer's disease and frontotemporal lobar degeneration. Nat Med. 2020 mar;26(3):387-397.32123386
65. Mielke MM, Hagen CE, Xu J, et al. Plasma phospho-tau181 increases with Alzheimer's disease clinical severity and is associated with tau- and amyloid-positron emission tomography. Alzheimers Dement. 2018 Aug;14(8):989-997.29626426
66. Mielke MM, Hagen CE, Wennberg AMV, et al. Association of Plasma Total Tau Level With Cognitive Decline and Risk of Mild Cognitive Impairment or Dementia in the Mayo Clinic Study on Aging. JAMA Neurol. 2017 Sep 1;74(9):1073-1080.28692710
67. Tatebe H, Kasai T, Ohmichi T, et al. Quantification of plasma phosphorylated tau to use as a biomarker for brain Alzheimer pathology: pilot case-control studies including patients with Alzheimer's disease and down syndrome. Mol Neurodegener. 2017 Sep 4;12(1):63.28866979
68. Janelidze S, Mattsson N, Palmqvist S, et al. Plasma P-tau181 in Alzheimer's disease: relationship to other biomarkers, differential diagnosis, neuropathology and longitudinal progression to Alzheimer's dementia. Nat Med. 2020 Mar;26(3):379-386.32123385
69. Morrison MS, Aparicio HJ, Blennow K, et al. Ante-mortem plasma phosphorylated tau (181) predicts Alzheimer's disease neuropathology and regional tau at autopsy. Brain. 2022 Oct 21;145(10):3546-3557. Epub 2022 May 13.35554506
70. Moscoso A, Karikari TK, Grothe MJ, et al. CSF biomarkers and plasma p-tau181 as predictors of longitudinal tau accumulation: Implications for clinical trial design. Alzheimers Dement. 2022 Dec;18(12):2614-2626. Epub 2022 Feb 28.35226405
71. Tissot C, Benedet AL, Therriault J, et al. Plasma pTau181 predicts cortical brain atrophy in aging and Alzheimer's disease. Alzheimers Res Ther. 2021 Mar 29;13(1):69.33781319
72. Cullen NC, Leuzy A, Palmqvist S, et al. Individualized prognosis of cognitive decline and dementia in mild cognitive impairment based on plasma biomarker combinations. Nat Aging. 2021;1:114-123. doi.org/10.1038/s43587-020-00003-5

LOINC® Map

Order Code Order Code Name Order Loinc Result Code Result Code Name UofM Result LOINC
483745 p-tau181 103675-5 483746 p-tau181 pg/mL 103675-5

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