Plasma amyloid, tau, and neurodegeneration biomarker profiles predict Alzheimer's disease pathology and clinical progression in older adults without dementia
Open accessAbstract
Introduction Plasma markers have been reported to be associated with brain amyloid burden, tau pathology, or neurodegeneration. We aimed to evaluate whether plasma biomarker profiles could predict Alzheimer's disease (AD) pathology and clinical progression in older adults without dementia. Methods Cross-sectional and longitudinal data of participants enrolled in this study were from the Alzheimer's Disease Neuroimaging Initiative (ADNI). Plasma amyloid beta (Aβ)1-42/Aβ1-40 ratio was selected as the marker for amyloid pathology, p-tau181 for tau pathology, and neurofilament light for neurodegeneration. Cut-offs for these plasma markers were calculated with well-established positron emission tomography and structural imaging biomarkers as reference. Older adults without dementia were categorized into eight groups at baseline by plasma amyloid/tau/neurodegeneration (A/T/N) cut-offs. Clinical progression was analyzed using linear mixed-effects models and Cox proportional hazard models. Results A total of 183 participants (97 cognitively normal [CN] subjects and 86 patients with mild cognitive impairment [MCI]; mean age 72.6 years, and 48.1% men) were included. Participants with A+ had significantly higher proportions of apolipoprotein E (APOE) gene ɛ4 carriers than those with A–. Brain atrophy was observed in all groups of CN, whereas cognition decline was obvious in the A+T+N+ group. Compared to A–T–N–, MCI patients with A+T+N+ had faster cognition worsening and faster brain atrophy. In the whole cohort, A+T+N+ and A+T+N– participants were at higher risk of clinical progression. Discussion Plasma A/T/N biomarker profiles may predict AD pathology and clinical progression, indicating a potential role for plasma biomarkers in clinical trials. More research is warranted to develop a robust plasma AD framework.
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KP activation during viral infections such as VEEV may drive the pathological interplay of inflammation and KYN dysregulation in the development or exacerbation of neurodegeneration.
“This indicates KP activation during viral infections such as VEEV may drive the pathological interplay of inflammation and KYN dysregulation in the development or exacerbation of neurodegeneration [28,29,30].”
From VEEV TC-83 Triggers Dysregulation of the Tryptophan–Kynurenine Pathway in the Central Nervous System That Correlates with Cognitive Impairment in Tg2576 Mice (2024) · cites this paper as [28]
The Results and Discussion address Alzheimer’s biomarker profiles, brain atrophy, and clinical progression, not kynurenine-pathway activation during viral infection. Searches for VEEV, kynurenine/KYN dysregulation, and inflammation returned no passage addressing the proposed mechanism; the References mention an HIV study but do not establish the claim. (LLM, conf=0.76)
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“Furthermore, our previous study has demonstrated that the plasma p-tau181 could be utilized as a progression marker for clinical conversion and cognitive decline [31], and the present findings proved that it was also specific for the AD pathophysiological processes.”
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“Shen et al. (2020) used plasma biomarker to identify amyloid, tau, or neurodegeneration.”
MethodNeuropathology, Neuroimaging, and Fluid Biomarkers in Alzheimer’s Disease
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“Follow-up, median (months)*** 22 (0-67) 55 (34-91) 0 (0-18)”
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MethodIkanga, J. N., Patel, S. S., Roberts, B. R., Schwinne, M., Hickle, S. D., Verberk, I. M. W., Epenge, E., Gikelekele, G., Tshengele, N., Kavugho, I., et al. (2023) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.12496 · Cited by 14 · see citing works
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“Summary florbetapir standard uptake value ratios were acquired by averaging uptake ratios across cortical regions (frontal, anterior/posterior cingulate, lateral parietal, lateral temporal regions) normalized by the reference region (whole cerebellum) [27].”
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“In our study, we observed a decrease in plasma t-tau levels in the AD group, which differs from the trends observed in other research groups (Mattsson et al., 2016; Shen, 2020).”
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White, H., Webb, R., McKnight, I., Legg, K., Lee, C., Lee, P. H. U., Spicer, O. S., & Shim, J. W. (2022) · Frontiers in Genetics · doi:10.3389/fgene.2022.936151 · Cited by 10 · see citing works
“We confirmed the previous finding that MAPT and APP mRNA are elevated in the caudate nucleus (tissue), consistent with fluid assays of AD (Musiek and Holtzman, 2012; Lafirdeen et al., 2019; McLimans et al., 2019; Barthelemy et al., 2020; Shen et al., 2020; Shen et al., 2021).”
ResultLongitudinal changes in blood-borne geroscience biomarkers: results from a population-based study
Picca, A., Nguyen, N. V., Calvani, R., Dale, M., Fredolini, C., Marzetti, E., Calderón-Larrañaga, A., & Vetrano, D. (2025) · GeroScience · doi:10.1007/s11357-025-01666-x · Cited by 6 · see citing works
“An increase in circulating Tau protein is strongly associated with neurodegenerative diseases or traumatic brain injury [32–36].”
Ohara, T., Tatebe, H., Hata, J., Honda, T., Shibata, M., Matsuura, S., Mikami, T., Maeda, T., Ono, K., Mimura, M., et al. (2024) · Psychiatry and Clinical Neurosciences · doi:10.1111/pcn.13661 · Cited by 6 · see citing works
“9,11,12 Meanwhile, no prospective studies have assessed the association between plasma GFAP levels and risk of dementia.”
BackgroundComputer-based cognitive tests and cerebral pathology among Japanese older adults
Shimada, H., Makino, K., Kato, T., & Ito, K. (2023) · BMC Geriatrics · doi:10.1186/s12877-023-03918-x · Cited by 8 · see citing works
“According to recent studies, AD pathology can be defined by plasma amyloid, tau, and neurodegeneration biomarker profiles; these profiles exhibit promising accuracy for predicting clinical progression in older adults without dementia [4].”
BackgroundPiccirella, S., Uberti, D., Xiong, C., Fowler, C., Doecke, J., Fagan, A., Frisoni, G., & Kinnon, P. (2021) · Preprints.org · doi:10.20944/preprints202105.0267.v1 · Cited by 4 · see citing works
“Although ATN blood-based biomarkers were originally designed for diagnostic purposes, they were recently shown to accurately predict the clinical progression to AD dementia in non-demented adults and patients with MCI (46).”
BackgroundFongsaran, C., Dineley, K. T., Paessler, S., & Cisneros, I. E. (2024) · Pathogens · doi:10.3390/pathogens13050397 · Cited by 3 · see citing works
Prognostic value of plasma Aβ1-40 for Alzheimer's disease.
Lv, H., Tang, L., Jian, C.-D., Wei, A., Li, D.-X., Jiang, Y., Yang, C., Mo, S., Shang, J.-W., & Li, X.-Z. (2024) · American journal of translational research · doi:10.62347/piyv4216 · Cited by 2 · see citing works
“…recent in vitro and in vivo studies have shown that the abnormal expression of plasma β-amyloid may activate an inflamma - tory response, continuously activating inflam - matory repair mechanisms and transforming the acute response under normal conditions into chronic inflammatory injury [21-23].”
BackgroundAyele, B. A., Whitehead, P., Pascual, J., Gu, T., Rajabli, F., Arvizu, J., Golightly, C. G., Adams, L., Pericak-Vance, M., Vance, J., et al. (2025) · Journal of Alzheimer's Disease · doi:10.1177/13872877251364899 · Cited by 1 · see citing works
Alzheimer's disease plasma biomarkers in the Midwestern Amish
Wang, P., Song, Y. E., Lynn, A., Miskimen, K. L. S., Gulyayev, A. V., Prough, M. B., Dorfsman, D. A., Laux, R. A., Fuzzell, S. L., Hochstetler, S. D., et al. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70328 · Cited by 3 · see citing works
Saez-Calveras, N., Asturias, A., Yu, J., Stopschinski, B., Vaquer-Alicea, J., O'Suilleabhain, P., Mckenzie, L., Viera, J., Diamond, M. I., & Shah, B. R. (2024) · Brain Communications · doi:10.1093/braincomms/fcaf054 · Cited by 1 · see citing works
Self-citationHou, K., Lu, H., Zhang, R., Wang, Y., Xu, G., Long, F., Lu, J., Xing, D. M., Huang, L., Sun, Y., et al. (2026) · Journal of Alzheimer s Disease Reports · doi:10.1177/25424823261433955
Chi, D., Liang, X.-N., Xiao, Z.-X., Zhou, X.-W., Zhao, Q.-H., Wang, B., & Ding, D. (2025) · CNS Neuroscience & Therapeutics · doi:10.1002/cns.70691
Plasma Glial Fibrillary Acidic Protein (GFAP) as a Biomarker of Acute Focal Brain InjuryPreprint
Saez-Calveras, N., Asturias, A., Yu, J., Stopschinski, B., Vaquer-Alicea, J., O'Suilleabhain, P., Diamond, M. I., & Shah, B. R. (2024) · medRxiv · doi:10.1101/2024.10.11.24315320
“9,10 11,12 .”
Self-citationRecent progresses on p-tau as a blood-based Alzheimer’s disease biomarker
Sadala, D., Ramos, V., de Oliveira, D. D. S. M. S., Fernandes, M. J. D. S., & Cominetti, M. R. (2021) · Revista Neurociências · doi:10.34024/rnc.2021.v29.12512
- Authors
- Shen, X., Li, J., Wang, H., Li, H., Huang, Y., Yang, Y., Tan, L., Dong, Q., Yu, J., & Initiative, A. D. N.
- Affiliations
- Shanghai Medical College of Fudan University (CN)
- Department of Neurology the Affiliated Hospital of Qingdao University Qingdao China
- Qingdao University (CN)
- Department of Neurology and Institute of Neurology Huashan Hospital Shanghai Medical College Fudan University Shanghai China
- Corresponding author
- Yu, Jin‐Tai
- Venue
- Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring
- Publisher
- Wiley
- Published
- 2020-01
- Volume
- 12
- Issue
- 1
- Pages
- e12104-e12104
- ISSN
- 2352-8729 (ISSN-L)
- PMC
- PMC7513626
- OpenAlex
- W3087949202
- Cited by
- 57
- References
- 45
- Citations by year
- 2026: 1 · 2025: 7 · 2024: 12 · 2023: 15 · 2022: 11 · 2021: 10 · 2020: 1
- FWCI
- 6.75
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (91849126, 81571245, 81771148)
- 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
- Alzheimer's disease, plasma biomarkers, p-tau181, neurofilament light chain, neurodegeneration, amyloid pathology, tau pathology, mild cognitive impairment, cognitive decline, brain atrophy, APOE ε4, clinical progression, cognitively normal older adults, ADNI
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