A blood test could help predict Alzheimer's decline in healthy older people

Embargoed until: Publicly released: 2026-07-15 14:00

Australia; International; VIC

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A blood test, which looks at the levels of a protein called phosphorylated tau 217(p-tau217), may help predict how quickly someone with no brain function issues is likely to develop mental decline, according to international and Australian research. The researchers looked at data from six trials based in North America, Japan, and Australia, and found that people with the highest levels of p-tau217 had around a 38% risk of progressing to show mental impairment over five years, while those with the lowest levels had only a 12% risk. The authors say the findings support the potential of p-tau217 to be used to help predict and estimate the long-term risk of mental decline.

News release

From: JAMA

Prognostic Value of Blood-Based P-Tau217 Levels for Progression to Cognitive Impairment

JAMA
About The Study: A study in JAMA presented Wednesday, July 15, at the annual Alzheimer’s Association International Conference reports that a blood test measuring phosphorylated tau 217 (P‑tau217) in plasma can help estimate an individual’s risk of developing cognitive impairment over the following 2, 5, and 10 years.

Across six cohorts, higher p-tau217 levels were consistently associated with increased risk of progression to cognitive impairment in cognitively unimpaired older adults, and the association remained significant after adjustment for amyloid PET.

The findings support P‑tau217 as a marker linked to amyloid and tau-related disease processes. If ongoing secondary prevention trials demonstrate that early intervention can delay or prevent cognitive decline, blood‑based biomarkers like P‑tau217 could help identify individuals most likely to benefit, authors note.

However, current Alzheimer’s Association clinical practice guidelines recommend against testing cognitively unimpaired older adults outside research studies or clinical trials.

Authors emphasize that the risk estimates are based on selected research cohorts, with greater confidence in 5‑year than 10‑year projections, and that current models do not fully account for vascular comorbidities or competing risk of death; additionally, P-tau217 may not fully reflect non-Alzheimer contributors to cognitive impairment, such as vascular or other neurodegenerative processes.

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Research JAMA, Web page

Journal/
conference: JAMA

Research: Link to Paper 1 | Paper 2

Organisation/s: The University of Melbourne, Mass General Brigham, UCLA, USA

Funder: Analyses for this study were supported by grants from the NIH (R01AG079142, DP2AG082342). Data collection and sharing for this project were funded by the Alzheimer’s Disease Neuroimaging Initiative (ADNI; NIH grant U01 AG024904) and US Department of Defense ADNI (W81XWH-12-2-0012). ADNI was launched in 2003 as a public-private partnership led by principal investigator MichaelW.Weiner,MD. ADNI is funded by the NIA, the National Institute of Biomedical Imaging and Bioengineering (NIBIB), and through generous contributions from AbbVie, Alzheimer’s Association, Alzheimer’s Drug Discovery Foundation, Araclon Biotech, Bioclinica, Biogen, Bristol Myers Squibb, CereSpir, Cogstate, Eisai, Elan Pharmaceuticals, Eli Lilly, Euroimmun, F. Hoffmann-La Roche and its affiliate Genentech, Fujirebio, GE HealthCare, IXICO, Janssen Alzheimer Immunotherapy Research & Development, Johnson & Johnson Pharmaceutical Research & Development, Lumosity, Lundbeck, Merck, Meso Scale Diagnostics, NeuroRx Research, Neurotrack Technologies, Novartis, Pfizer, Piramal Imaging, Servier, Takeda, and Transition Therapeutics. The Canadian Institutes of Health Research provides funds to support ADNI clinical sites in Canada. Private sector contributions are facilitated by the Foundation for the NIH (www.fnih.org). The grantee organization is the Northern California Institute for Research and Education, and the study was coordinated by the Alzheimer’s Therapeutic Research Institute at the University of Southern California. ADNI data are disseminated by the Laboratory for Neuro Imaging at the University of Southern California. Research reported in this article was supported by the NIA of the NIH (R01AG054073, R01AG058533, R01AG070862, P41EB015922, U19AG078109). HABS-HD was supported by the NIA of the NIH (R01AG054073, R01AG058533, R01AG070862, P41EB015922, U19AG078109). WRAP was supported by the NIH (R01AG027161, R01AG021155, P30AG062715). The A4/LEARN studies were funded by the NIA (U19AG010483, R01AG063689), Eli Lilly, and several philanthropic organizations. The A4 study is funded by a public-private philanthropic partnership, including funding from the NIH/NIA (U19AG010483, R01AG063689), Eli Lilly, Alzheimer’s Association, Accelerating Medicines Partnership, GHR Foundation, an anonymous foundation, and additional private donors, with in-kind support from Avid, Cogstate, Albert Einstein College of Medicine, and Foundation for Neurologic Diseases. The companion observational LEARN study is funded by the Alzheimer’s Association and GHR Foundation. HABS is supported by the NIH (P01 AG036694). This research was conducted in part at the Athinoula A. Martinos Center for Biomedical Imaging at Massachusetts General Hospital, using resources provided by the Center for Functional Neuroimaging Technologies (P41EB015896), a P41 Biotechnology Resource Grant supported by NIBIB of the NIH. This work also involved the use of instrumentation supported by the NIH Shared Instrumentation Grant Program and/or High-End Instrumentation Grant Program (S10RR021110, S10RR023401, S10RR023043). The MIND Biomarker Core is partially funded by the NIA (P30AG062421). Meso Scale Diagnostics provided assay kits to measure p-tau217 in the HABS cohort free of charge.

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