Association of plasma P-tau181 with memory decline in non-demented adults
Open accessAbstract
Alzheimer’s disease is the leading cause of dementia worldwide and is characterized by a long preclinical phase in which amyloid-β and tau accumulate in the absence of cognitive decline. In vivo biomarkers for Alzheimer’s disease are expensive, invasive and inaccessible, yet are critical for accurate disease diagnosis and patient management. Recent ultrasensitive methods to measure plasma phosphorylated tau 181 (p-tau181) display strong correlations with tau positron emission tomography, p-tau181 in CSF, and tau pathology at autopsy. The clinical utility of plasma-based p-tau181 biomarkers is unclear. In a longitudinal multicentre observational study, we assessed 1113 non-demented individuals (509 cognitively unimpaired elderly and 604 individuals with mild cognitive impairment) from the Alzheimer’s Disease Neuroimaging Initiative who underwent neuropsychological assessments and were evaluated for plasma p-tau181. The primary outcome was a memory composite z-score. Mixed-effect models assessed rates of memory decline in relation to baseline plasma p-tau181, and whether plasma p-tau181 significantly predicted memory decline beyond widely available clinical and genetic data (age, sex, years of education, cardiovascular and metabolic conditions, and APOEε4 status). Participants were followed for a median of 4.1 years. Baseline plasma p-tau181 was associated with lower baseline memory (β estimate: −0.49, standard error: 0.06, t-value: −7.97), as well as faster rates of memory decline (β estimate: −0.11, standard error: 0.01, t-value: −7.37). Moreover, the inclusion of plasma p-tau181 resulted in improved prediction of memory decline beyond clinical and genetic data (marginal R2 of 16.7–23%, χ2 = 100.81, P < 0.00001). Elevated baseline plasma p-tau181 was associated with higher rates of clinical progression to mild cognitive impairment (hazard ratio = 1.82, 95% confidence interval: 1.2–2.8) and from mild cognitive impairment to dementia (hazard ratio = 2.06, 95% confidence interval: 1.55–2.74). Our results suggest that in elderly individuals without dementia at baseline, plasma p-tau181 biomarkers were associated with greater memory decline and rates of clinical progression to dementia. Plasma p-tau181 improved prediction of memory decline above a model with currently available clinical and genetic data. While the clinical importance of this improvement in the prediction of memory decline is unknown, these results highlight the potential of plasma p-tau181 as a cost-effective and scalable Alzheimer’s disease biomarker.
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Blood measures of p-tau181, p-tau217, p-tau231, GFAP, NfL and Aβ42/40 have been shown to change in preclinical AD and can discriminate this state from CU individuals with non-AD pathological changes.
“Indeed, blood measures of p-tau181, p-tau217, p-tau231, glial fibrillary acid protein (GFAP), neurofilament light (NfL) and Aβ42/40 have been shown to change in preclinical AD and can discriminate this state from CU individuals with non-AD pathological changes1,3,6–13.”
From Plasma p-tau231 and p-tau217 as state markers of amyloid-β pathology in preclinical Alzheimer’s disease (2022) · cites this paper as [10]
The Discussion (page not specified in our copy) describes plasma p-tau181 as specific for Alzheimer’s disease tau pathology and notes that it becomes abnormal after amyloid-β does. That supports the p-tau181 portion, but the paper does not show that the full listed panel discriminates preclinical AD from cognitively unimpaired people with non-AD pathological changes; it discusses several other markers only as potential additions or in references. (LLM, conf=0.85)
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“22,25,29,32,54,55 Ofnote,Tertile-3p-tau181wasassociatedwithfastermemorydecline, consistent with its role as an ADRD biomarker.”
BackgroundSelf-citationTwo-Year Prognostic Utility of Plasma p217+tau across the Alzheimer's Continuum
Feizpour, A., Doré, V., Doecke, J. D., Saad, Z. S., Triana‐Baltzer, G., Slemmon, R., Maruff, P. T., Krishnadas, N., Bourgeat, P., Huang, K., et al. (2023) · The Journal of Prevention of Alzheimer s Disease · doi:10.14283/jpad.2023.83 · Cited by 21 · see citing works
“Therriault et al. (30) also reported a much lower β estimate of -0.01 for the association between baseline plasma p-tau181 status using Simoa® and longitudinal decline in memory in CU participants while the association between the same variables in the MCI group gave a β estimate of -0.12.”
ResultInfluentialDifferential roles of Alzheimer's disease plasma biomarkers in stepwise biomarker‐guided diagnostics
Jang, H., Shin, D., Yoo, H., Zetterberg, H., Blennow, K., González‐Ortiz, F., Ashton, N. J., Day, T. A., Lee, E. H., Yun, J., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.14526 · Cited by 26 · see citing works
“27,28 38 Finally, the biomarkers predicting prognosis may vary by cognitive stage and causes of CI.”
Self-citationPresent and Future of Blood-Based Biomarkers of Alzheimer’s Disease: Beyond the Classics
Grigoli, M. M., Pelegrini, L. N. D. C., Whelan, R., & Cominetti, M. R. (2024) · Brain Research · doi:10.1016/j.brainres.2024.148812 · Cited by 23 · see citing works
Prognostic and Predictive Factors in Early Alzheimer’s Disease: A Systematic Review
Garcia, M. J., Leadley, R. M., Ross, J., Bozeat, S., Redhead, G., Hansson, O., Iwatsubo, T., Villain, N., & Cummings, J. L. (2024) · Journal of Alzheimer s Disease Reports · doi:10.3233/adr-230045 · Cited by 53 · see citing works
Grasset, L., Bouteloup, V., Cacciamani, F., Pellegrin, I., Planche, V., Chêne, G., Dufouil, C., & for the MEMENTO study group (2024) · Neurology · doi:10.1212/wnl.0000000000209307 · Cited by 23 · see citing works
González‐Escalante, A., Milà‐Alomà, M., Brum, W. S., Ashton, N. J., Ortiz-Romero, P. L., Shekari, M., del Campo, M., Anastasi, F., Quijano‐Rubio, C., Kollmorgen, G., et al. (2025) · EBioMedicine · doi:10.1016/j.ebiom.2025.105741 · Cited by 24 · see citing works
Self-citationHuang, Y., Li, Y., Xie, F., & Guo, Q. (2022) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.13962 · Cited by 19 · see citing works
Lombardi, G., Pancani, S., Manca, R., Mitolo, M., Baiardi, S., Massa, F., Coppola, L., Franzese, M., Nicolai, E., Guerini, F. R., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252312916 · Cited by 18 · see citing works
“References [84–86]”
Medial temporal tau predicts memory decline in cognitively unimpaired elderly
Kwan, A. T. H., Arfaie, S., Therriault, J., Azizi, Z., Lussier, F. Z., Tissot, C., Chamoun, M., Bezgin, G., Servaes, S., Stevenon, J., et al. (2022) · Brain Communications · doi:10.1093/braincomms/fcac325 · Cited by 15 · see citing works
“tecting biological Alzheimer’s disease in vivo and during the preclinical phase.(8)”
BackgroundSelf-citationQuispialaya, K. M., Therriault, J., Aliaga, A., Tissot, C., Servaes, S., Rahmouni, N., Karikari, T. K., Benedet, A. L., Ashton, N. J., Macedo, A. C., et al. (2024) · European Journal of Neurology · doi:10.1111/ene.16255 · Cited by 12 · see citing works
Self-citationPlasma p-tau181 associated with structural changes in mild cognitive impairment
Nabizadeh, F., Balabandian, M., Rostami, M. R., Ward, R. T., Ahmadi, N., Pourhamzeh, M., & Initiative, A. D. N. (2022) · Aging Clinical and Experimental Research · doi:10.1007/s40520-022-02148-2 · Cited by 9 · see citing works
Zhang, S., Wang, F., Xie, L., Xu, J., Song, X., Tao, J., Chen, J., Ma, D., Yu, X., Shi, X., et al. (2024) · Journal of Diabetes Investigation · doi:10.1111/jdi.14306 · Cited by 7 · see citing works
Borelli, W. V., Ferreira, P. C. L., Brum, W. S., Ferrari‐Souza, J. P., Carello‐Collar, G., Holz, M. R., Souza, V. T., Strelow, M. Z., Formoso, C., Chaves, M. L. F., et al. (2025) · Molecular Psychiatry · doi:10.1038/s41380-025-03192-w · Cited by 8 · see citing works
Self-citationReal‐world performance of plasma p‐tau181 in a heterogeneous memory clinic cohort
Parvizi, T., Wurm, R., König, T., Silvaieh, S., Altmann, P., Klotz, S., Regelsberger, G., Traub‐Weidinger, T., Gelpí, E., & Stögmann, E. (2024) · Annals of Clinical and Translational Neurology · doi:10.1002/acn3.52116 · Cited by 5 · see citing works
“49 – 51 Due to the fact, that the addition of APOE4 to plasma p-tau181 in our ROC analyses did not show a significant advantage compared with plasma p-tau181 and age, we constructed a model based on plasma p-tau181 levels, MMSE and age to calculate the probability of having an abnormal cerebral…”
MethodWang, S., Ke, S., Liu, S., Wang, E., & Pan, T. (2023) · Neuroscience Letters · doi:10.1016/j.neulet.2023.137052 · Cited by 5 · see citing works
Bolton, C. J., Steinbach, M., Khan, O. A., Liu, D., O’Malley, J., Dumitrescu, L. C., Peterson, A. J., Jefferson, A. L., Hohman, T. J., Zetterberg, H., et al. (2024) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.70047 · Cited by 4 · see citing works
Self-citationPais, M. V., Kuo, C., Ances, B. M., Wetherell, J. L., Lenze, E. J., & Diniz, B. S. (2023) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.12487 · Cited by 4 · see citing works
Li, J., Wu, C., Liu, Q., Liu, M., Liu, T., Li, A., Fu, G., Zou, Z., Guo, D., Chen, K., et al. (2025) · iScience · doi:10.1016/j.isci.2025.113168 · Cited by 3 · see citing works
“57,58 In summary, we hypothesize that pathological changes in AD first manifest in peripheral systems, subsequently progressing to the central nervous system, leading to brain pathology and cognitive decline.”
Contingency of Plasma Dementia Biomarkers on Cognitive Profiles for Prognosis of Incident Dementia
Knopman, D. S., Pike, J. R., Griswold, M., Lu, Y., Gross, A. L., Mosley, T. H., Windham, B. G., Albert, M., Walker, K. A., Gottesman, R. F., et al. (2026) · Neurology · doi:10.1212/wnl.0000000000214779 · Cited by 2 · see citing works
Cai, Y., Fu, P., & Zhang, X. (2023) · Neuroscience Letters · doi:10.1016/j.neulet.2023.137161 · Cited by 2 · see citing works
“Consistent with previous literature, plasma p-tau181 correlates with β -amyloid pathology and is a promising biomarker for clinical diagnosis [4,27 – 29].”
Applications of Alzheimer’s disease staging to clinical trials
Therriault, J., Gauthier, S. G., & Rosa‐Neto, P. (2023) · Aging · doi:10.18632/aging.204482 · Cited by 2 · see citing works
Self-citationPotential utility of plasma p-tau and NfL as surrogate biomarkers for preventive clinical trialsPreprint
Ferreira, P. C. L., Ferrari‐Souza, J. P., Tissot, C., Bellaver, B., Leffa, D. T., Lussier, F. Z., Povala, G., Therriault, J., Benedet, A. L., Ashton, N. J., et al. (2022) · medRxiv · doi:10.1101/2022.08.17.22278853 · Cited by 1 · see citing works
Self-citationDiagnostic performance of Alzheimer’s disease blood biomarkers in a Brazilian cohortPreprint
Borelli, W. V., Ferreira, P. C. L., Brum, W. S., Ferrari‐Souza, J. P., Carello‐Collar, G., Holz, M. R., Souza, V. T., Strelow, M. Z., Formoso, C., Chaves, M. L. F., et al. (2025) · medRxiv · doi:10.1101/2025.02.23.24319116 · Cited by 1 · see citing works
Self-citationSaunders, T. S., Heslegrave, A., King, D., Harris, S. E., Ritchie, C. W., Terrera, G. M., Deary, I. J., Cox, S. R., Zetterberg, H., & Spires‐Jones, T. L. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.11.24.469836
“Both CSF and plasma p-tau181 concentrations are elevated in AD relative to controls [12] and have been found to correlate with global cognitive function in those with mild cognitive impairment (MCI) [13].”
MethodSelf-citationWang, S., Initiative, A. D. N., Liu, S., Ke, S., Zhou, W., & Pan, T. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230437 · Cited by 1 · see citing works
Zhang, S., Shi, X., Zheng, S., Liang, X., Wang, F., Xu, W., Yu, X., & Yang, Y. (2025) · Journal of Diabetes Research · doi:10.1155/jdr/8029913
Kelleher-Andersson, J. A., Yoon, E., Green, C., McFarlane, C., Bagheri, D., Thomas, L. P., & Turner, R. S. (2025) · Alzheimer s Research & Therapy · doi:10.1186/s13195-025-01837-0
“Recent clinical findings concluded that differences in baseline levels of p-tau 181 in elderly subjects (> 70 years of age) was associated with memory deficit [14].”
Stringhi, R., Pelucchi, S., D’Andrea, L., Greca, F. L., Zianni, E., Targa, L., Mosconi, C., Vandermeulen, L., Ascagni, M., Speciani, M. C., et al. (2025) · Molecular Therapy · doi:10.1016/j.ymthe.2025.12.023
Wilson, E. N., Young, C. B., Benitez, J. A. R., Swarovski, M. S., Feinstein, I., Vandijck, M. L. J., Guen, Y. L., Kasireddy, N. M., Shahid, M., Corso, N. K., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21547387
Wilson, E. N., Young, C. B., Benitez, J. A. R., Swarovski, M. S., Feinstein, I., Vandijck, M. L. J., Guen, Y. L., Kasireddy, N. M., Shahid, M., Corso, N. K., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21547393
Wilson, E. N., Young, C. B., Benitez, J. A. R., Swarovski, M. S., Feinstein, I., Vandijck, M. L. J., Guen, Y. L., Kasireddy, N. M., Shahid, M., Corso, N. K., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21547396
Wilson, E. N., Young, C. B., Benitez, J. A. R., Swarovski, M. S., Feinstein, I., Vandijck, M. L. J., Guen, Y. L., Kasireddy, N. M., Shahid, M., Corso, N. K., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21547390
Wilson, E. N., Young, C. B., Benitez, J. A. R., Swarovski, M. S., Feinstein, I., Vandijck, M. L. J., Guen, Y. L., Kasireddy, N. M., Shahid, M., Corso, N. K., et al. (2022) · Figshare · doi:10.6084/m9.figshare.21547384
Circulating pTau181 and Genomic Background in Dogs: A Pilot Study on Neurobiological Aging
Gazzano, V., Fabbri, M. C., Capsoni, S., Cantile, C., Tinacci, L., Gazzano, A., Curadi, M. C., & Cecchi, F. (2026) · Veterinary Medicine International · doi:10.1155/vmi/7159552
Comparative analyses of Alzheimer's disease blood biomarkers and cognitive domains
O’Shea, D. M., & Galvin, J. E. (2026) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.70471
“18,20,35”
- Authors
- Therriault, J., Benedet, A. L., Pascoal, T. A., Lussier, F. Z., Tissot, C., Karikari, T. K., Ashton, N. J., Chamoun, M., Bezgin, G., Mathotaarachchi, S., Gauthier, S., Saha-Chaudhuri, P., Zetterberg, H., Blennow, K., Rosa-Neto, P., & Initiative, F. T. A. D. N.
- Affiliations
- McGill University (CA)
- Translational Neuroimaging Laboratory, McGill University, Montreal, Canada
- Sahlgrenska University Hospital (SE)
- King's College London (GB)
- Department of Epidemiology and Biostatistics, McGill University, Montreal, Canada
- ORCID
- Venue
- Brain Communications
- Publisher
- Oxford University Press (OUP)
- Published
- 2021-06-14
- Volume
- 3
- Issue
- 3
- Pages
- fcab136-fcab136
- ISSN
- 2632-1297 (ISSN-L)
- PMC
- PMC8249102
- OpenAlex
- W3166886117
- Cited by
- 56
- References
- 46
- Citations by year
- 2026: 3 · 2025: 9 · 2024: 13 · 2023: 12 · 2022: 17 · 2021: 2
- FWCI
- 7.89
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Brain Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- Canadian Institutes of Health Research (MOP-11–51-3)
- Alzheimer’s Association (NIRG-12–92090, NIRP-12–259245)
- Fonds de Recherche du Québec–Santé (2020-VICO-279314)
- Weston Brain Foundation
- Swedish Research Council (#2018–02532, #2017–00915)
- European Research Council (#681712)
- Swedish State Support for Clinical Research (#ALFGBG-720931)
- Alzheimer Drug Discovery Foundation (ADDF), USA (#201809–2016862, #RDAPB-201809–2016615)
- UK Dementia Research Institute
- Swedish Alzheimer Foundation (#AF-742881)
- Hjärnfonden, Sweden (#FO2017-0243)
- Swedish government and the County Councils, the ALF-agreement (#ALFGBG-715986)
- European Union Joint Program for Neurodegenerative Disorders (JPND2019-466–236)
- 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 › Pulmonary and Respiratory Medicine › Cancer-related cognitive impairment studies
- Keywords
- p-tau181, Alzheimer's disease, memory decline, mild cognitive impairment, dementia progression, plasma biomarkers, preclinical Alzheimer's disease, APOE ε4, cognitive aging, Alzheimer's Disease Neuroimaging Initiative, tau pathology, amyloid-beta deposition
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