Diagnostic value of plasma phosphorylated tau181 in Alzheimer's disease and frontotemporal lobar degeneration
Open accessAbstract
With the potential development of new disease-modifying Alzheimer’s disease (AD) therapies, simple, widely available screening tests are needed to identify which individuals, who are experiencing symptoms of cognitive or behavioral decline, should be further evaluated for initiation of treatment. A blood-based test for AD would be a less invasive and less expensive screening tool than the currently approved cerebrospinal fluid or amyloid β positron emission tomography (PET) diagnostic tests. We examined whether plasma tau phosphorylated at residue 181 (pTau181) could differentiate between clinically diagnosed or autopsy-confirmed AD and frontotemporal lobar degeneration. Plasma pTau181 concentrations were increased by 3.5-fold in AD compared to controls and differentiated AD from both clinically diagnosed (receiver operating characteristic area under the curve of 0.894) and autopsy-confirmed frontotemporal lobar degeneration (area under the curve of 0.878). Plasma pTau181 identified individuals who were amyloid β-PET-positive regardless of clinical diagnosis and correlated with cortical tau protein deposition measured by 18F-flortaucipir PET. Plasma pTau181 may be useful to screen for tau pathology associated with AD. Plasma pTau181 concentrations are elevated specifically in patients diagnosed with Alzheimer’s disease compared to those diagnosed with frontotemporal lobar degeneration or elderly controls, supporting its further development as a blood-based biomarker for AD.
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Plasma phosphorylated tau at threonine 181 separates autopsy-confirmed Alzheimer disease from frontotemporal lobar degeneration better than clinical or amyloid PET-based classification.
“We also recently observed that phosphorylated plasma tau at threonine 181 differentiates autopsy-diagnosed AD from FTLD with better accuracy than clinically diagnosed or amyloid PET-defined cases.22”
From Plasma Tau and Neurofilament Light in Frontotemporal Lobar Degeneration and Alzheimer Disease (2021) · cites this paper as [22]
The Discussion (page not supplied) says the opposite of the claimed comparison: plasma pTau181 differentiated autopsy-diagnosed AD from FTLD with slightly lower accuracy than in clinically diagnosed or PET-defined cases. (LLM, conf=0.95)
Checked by a reasoning model — may be wrong.
Experimental — accuracy not yet measuredSeveral recent studies have reported that plasma biomarkers have excellent diagnostic accuracy for AD, with sensitivity or specificity often exceeding 90%.
“Several recent studies have reported that plasma biomarkers have excellent diagnostic accuracy for AD, with sensitivity or specificity often exceeding 90% (refs. 4–10).”
From Diagnosis of Alzheimer's disease using plasma biomarkers adjusted to clinical probability (2024) · cites this paper as [4]
The Results report that plasma pTau181 differentiated clinically diagnosed AD from FTLD, and Extended Data Fig. 6 reports 94.4% sensitivity for identifying amyloid-PET positivity in patients with mild cognitive impairment. That figure concerns PET status rather than a clinical AD diagnosis; the Discussion describes sensitivity and specificity for differentiating AD from FTLD as similar to approximately 70–80%. This paper therefore supports strong diagnostic performance and one sensitivity above 90%, but not the broader implication that sensitivity or specificity often exceeds 90% for diagnosing AD. (LLM, conf=0.84)
Experimental — accuracy not yet measuredPlasma levels of p-tau are strongly associated with PET and CSF biomarkers of AD pathology, neuropathological changes associated with AD, and subsequent development of AD dementia.
“Plasma levels of p-tau are strongly associated with PET and CSF biomarkers of AD pathology19–25, neuropathological changes associated with AD20,23,26,27 and the subsequent development of AD dementia20,23,28.”
From Highly accurate blood test for Alzheimer's disease is similar or superior to clinical cerebrospinal fluid tests (2024) · cites this paper as [24]
The Results section reports strong associations between plasma pTau181 and amyloid- and tau-PET measures; the Discussion also reports associations with CSF pTau181 and autopsy-assessed AD tau pathology. The Discussion says plasma pTau181 predicted clinical and neuropsychological decline over two years in participants with clinical AD or MCI, but our copy does not establish that it predicted subsequent development of AD dementia. Page numbers are unavailable in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredPlasma phosphorylated tau at residues 181 or 217 has similar diagnostic accuracy to amyloid and tau PET or CSF measures for the differential diagnosis from Alzheimer's disease.
“Plasma measures of phos phorylated tau at residues 181 or 217 have similar diagnostic accuracy to amyloid and tau PET or CSF measures for the differential diagnosis from Alzheimer's disease, and plasma phosphorylated tau measures might eventually supplant these”
From Advances and controversies in frontotemporal dementia: diagnosis, biomarkers, and therapeutic considerations (2022) · cites this paper as [49]
The Discussion says plasma pTau181 differentiated Alzheimer’s disease from frontotemporal lobar degeneration with accuracy similar to previously reported amyloid-PET accuracy, and reports accuracy similar to CSF pTau181. The paper also relates pTau181 to tau-PET findings, but the cited passages do not establish similar differential-diagnostic accuracy to tau PET. It studies pTau181, not pTau217; no page numbers are available in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredTotal tau and amyloid β concentrations are not sensitive or specific for any of the frontotemporal lobar degeneration proteinopathies.
“Although total tau and amyloid β concentrations are not sensitive or specific for any of the frontotemporal lobar degeneration proteinopathies, elevated phosphorylated tau concentrations in either CSF or plasma suggest that underlying Alzheimer's disease pathology is likely to be the cause of the frontotemporal dementia clinical syndrome.49,55,56”
From Advances and controversies in frontotemporal dementia: diagnosis, biomarkers, and therapeutic considerations (2022) · cites this paper as [49]
The Discussion says CSF total tau has little diagnostic value for distinguishing FTLD from Alzheimer’s disease. The Results report that plasma Aβ42/40 did not differ between clinical diagnostic groups. These findings support limited diagnostic usefulness, but the paper does not establish that total tau and amyloid β concentrations lack sensitivity or specificity for every FTLD proteinopathy. (LLM, conf=0.83)
Experimental — accuracy not yet measured
Elevated phosphorylated tau concentrations in either CSF or plasma suggest that underlying Alzheimer's disease pathology is likely to be the cause of the frontotemporal dementia clinical syndrome.
“Although total tau and amyloid β concentrations are not sensitive or specific for any of the frontotemporal lobar degeneration proteinopathies, elevated phosphorylated tau concentrations in either CSF or plasma suggest that underlying Alzheimer's disease pathology is likely to be the cause of the frontotemporal dementia clinical syndrome.49,55,56”
From Advances and controversies in frontotemporal dementia: diagnosis, biomarkers, and therapeutic considerations (2022) · cites this paper as [49]
The Discussion (page not supplied) says elevated plasma pTau181 helps distinguish AD from FTLD, and the Results report higher CSF pTau181 in clinically diagnosed AD than in FTLD. But the Discussion also reports elevated plasma pTau181 in some MAPT-related FTLD without amyloid pathology. Thus elevation can suggest AD, but this paper does not establish that AD is likely to be the cause of every frontotemporal dementia syndrome with elevated pTau. (LLM, conf=0.83)
Experimental — accuracy not yet measuredCSF NfL is elevated in frontotemporal lobar degeneration, but its concentrations do not differentiate frontotemporal lobar degeneration from non-frontotemporal lobar degeneration pathology, nor do they distinguish the different proteinopathies in frontotemporal lobar degeneration.
“NfL in CSF is elevated in frontotemporal lobar degeneration, but concentrations do not differentiate frontotemporal lobar degeneration from non-frontotemporal lobar degeneration pathology, nor do they distinguish the different protein opathies in frontotemporal lobar degeneration.47,49,50”
From Advances and controversies in frontotemporal dementia: diagnosis, biomarkers, and therapeutic considerations (2022) · cites this paper as [49]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredPhosphorylated tau 181 (P-tau181) gets deposited in the brain and secreted in CSF which crosses the blood brain barrier to enter the blood where it can be used as a biomarker for Alzheimer's disease.
“It gets deposited in the brain and secreted in CSF which crosses blood brain barrier to enter the blood where it can be used as a biomarker for AD [35, 36].”
From Recent Advancements in Pathogenesis, Diagnostics and Treatment of Alzheimer’s Disease (2020) · cites this paper as [36]
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Self-citationCSF neurofilament light chain and phosphorylated tau 181 predict disease progression in PSP
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Self-citationFlortaucipir F 18 quantitation using parametric estimation of reference signal intensity.
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Self-citationSwine flu snipers, Alzheimer’s drug push and Google’s latest gaming bot
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Self-citationThe informed road map to prevention of Alzheimer Disease: a call to arms
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Self-citationAnti‐amyloid antibody treatments for Alzheimer's disease
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Self-citationPlasma Phospho‐Tau Identifies Alzheimer's Co‐Pathology in Patients with Lewy Body Disease
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Self-citationCerebrovascular Senescence Is Associated With Tau Pathology in Alzheimer's Disease
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Self-citationPre‐diagnostic cognitive and functional impairment in multiple sporadic neurodegenerative diseases
Swaddiwudhipong, N., Whiteside, D. J., Hezemans, F. H., Street, D., Rowe, J. B., & Rittman, T. (2023) · Alzheimer's & Dementia · doi:10.1002/alz.12802 · Cited by 48 · see citing works
Salvadó, G., Larsson, V., Cody, K. A., Cullen, N. C., Jonaitis, E. M., Stomrud, E., Kollmorgen, G., Wild, N., Palmqvist, S., Janelidze, S., et al. (2023) · Alzheimer's & Dementia · doi:10.1002/alz.12907 · Cited by 46 · see citing works
Self-citationAsken, B. M., Tanner, J. A., VandeVrede, L., Mantyh, W. G., Casaletto, K. B., Staffaroni, A. M., La Joie, R., Iaccarino, L., Soleimani-Meigooni, D., Rojas, J. C., et al. (2022) · Neurology · doi:10.1212/wnl.0000000000200678 · Cited by 40 · see citing works
Self-citationAnother step forward in blood-based diagnostics for Alzheimer’s disease
Bateman, R. J., Barthélemy, N. R., & Horie, K. (2020) · Nature Medicine · doi:10.1038/s41591-020-0797-4 · Cited by 37 · see citing works
Blood biomarkers in frontotemporal dementia: Review and meta-analysis
Ntymenou, S., Tsantzali, I., Kalamatianos, T., Voumvourakis, K. I., Kapaki, E., Tsivgoulis, G., Stranjalis, G., & Paraskevas, G. P. (2021) · Brain Sciences · doi:10.3390/brainsci11020244 · Cited by 31 · see citing works
Phosphorylated Tau 181 Serum Levels Predict Alzheimer’s Disease in the Preclinical Stage
Qin, W., Li, F., Jia, L., Wang, Q., Li, Y., Wei, Y., Li, Y., Jin, H., & Jia, J. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.900773 · Cited by 23 · see citing works
Chen, Y., Wang, Y., Tao, Q., Lu, P., Meng, F., Zhuang, L., Qiao, S., Zhang, Y., Luo, B., Liu, Y., et al. (2024) · Clinica Chimica Acta · doi:10.1016/j.cca.2024.118784 · Cited by 21 · see citing works
- Authors
- Advancing Research and Treatment for Frontotemporal Lobar Degeneration (ARTFL) investigators, Thijssen, E. H., La Joie, R., Wolf, A., Strom, A., Wang, P., Iaccarino, L., Bourakova, V., Cobigo, Y., Heuer, H., Spina, S., VandeVrede, L., Chai, X., Proctor, N. K., Airey, D. C., Shcherbinin, S., Duggan Evans, C., Sims, J. R., Zetterberg, H., Blennow, K., Karydas, A. M., Teunissen, C. E., Kramer, J. H., Grinberg, L. T., Seeley, W. W., Rosen, H., Boeve, B. F., Miller, B. L., Rabinovici, G. D., Dage, J. L., Rojas, J. C., & Boxer, A. L.
- Affiliations
- University of California, San Francisco (US)
- Eli Lilly (United States) (US)
- Sahlgrenska University Hospital (SE)
- Amsterdam Neuroscience (NL)
- Mayo Clinic (US)
- Corresponding author
- Boxer, Adam L.
- ORCID
- Thijssen, Elisabeth H.
- La Joie, Renaud
- Wolf, Amy
- Strom, Amelia
- Wang, Ping
- Iaccarino, Leonardo
- Cobigo, Yann
- Heuer, Hilary
- Spina, Salvatore
- VandeVrede, Lawren
- Proctor, Nicholas K.
- Shcherbinin, Sergey
- Sims, John R.
- Zetterberg, Henrik
- Blennow, Kaj
- Teunissen, Charlotte E.
- Kramer, Joel H.
- Grinberg, Lea T.
- Seeley, William W.
- Boeve, Bradley F.
- Miller, Bruce L.
- Rabinovici, Gil D.
- Dage, Jeffrey L.
- Rojas, Julio C.
- Boxer, Adam L.
- Venue
- Nature Medicine
- Published
- 2020-03
- Volume
- 26
- Issue
- 3
- Pages
- 387-397
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC7101073
- OpenAlex
- W3009833354
- Semantic Scholar
- 274c28c8529beee9e8a31454021c208f7d4ccb2c
- Cited by
- 761
- References
- 82
- Citations by year
- 2026: 58 · 2025: 96 · 2024: 116 · 2023: 124 · 2022: 157 · 2021: 130 · 2020: 77
- FWCI
- 88.99
- Type
- journal article
- Language
- en
- Open access
- green
- pure.amsterdamumc.nl
- Licence
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion, other-oa)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- Alzheimer's Association (K24AG053435, P50 AG023501, 443577, K23AG059888, AARF-16-443577, 16-443577)
- Eli Lilly and Company
- Biogen
- Rare Diseases Clinical Research Network
- Göteborgs Universitet
- Avid Radiopharmaceuticals (AV-1451)
- National Institute on Aging (K08AG052648, K23AG059888, R01AG045611, R01AG062268, P01AG066597, U01AG045390, RF1AG050967, K24AG045333, R01AG038791, U19AG063911, P01AG019724, K24AG053435, P30AG062422, P30AG062677, U24AG021886, T32AG023481, P50AG023501, P50AG016574)
- National Institute of Mental Health (R01MH120794)
- National Institute of Neurological Disorders and Stroke (U54NS092089)
- National Center for Advancing Translational Sciences (U24 AG21886)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- Alzheimer's disease, frontotemporal lobar degeneration, phosphorylated tau 181, plasma biomarkers, blood-based diagnosis, amyloid PET, tau pathology, differential diagnosis, disease screening
- MeSH terms
- Aged, Alzheimer Disease, Amyloid, Cognition, Female, Heterozygote, Humans, Male, Middle Aged, Mutation, Phosphorylation, Severity of Illness Index, Biomarkers, Amyloid beta-Peptides, tau Proteins, Neurofilament Proteins, Positron-Emission Tomography, Frontotemporal Lobar Degeneration, Gray Matter
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