Associations of amyloid, tau, and neurodegeneration biomarker profiles with rates of memory decline among individuals without dementia
Open accessAbstract
Importance: A National Institute on Aging and Alzheimer's Association workgroup proposed a research framework for Alzheimer disease in which biomarker classification of research participants is labeled AT(N) for amyloid, tau, and neurodegeneration biomarkers. Objective: To determine the associations between AT(N) biomarker profiles and memory decline in a population-based cohort of individuals without dementia age 60 years or older, and to determine whether biomarkers provide incremental prognostic value beyond more readily available clinical and genetic information. Design, Setting, and Participants: Population-based cohort study of cognitive aging in Olmsted County, Minnesota, that included 480 nondemented Mayo Clinic Study of Aging participants who had a clinical evaluation and amyloid positron emission tomography (PET) (A), tau PET (T), and magnetic resonance imaging (MRI) cortical thickness (N) measures between April 16, 2015, and November 1, 2017, and at least 1 clinical evaluation follow-up by November 12, 2018. Exposures: Age, sex, education, cardiovascular and metabolic conditions score, APOE genotype, and AT(N) biomarker profiles. Each of A, T, or (N) can be abnormal (+) or normal (-), resulting in 8 AT(N) profiles. Main Outcomes and Measures: Primary outcome was a composite memory score measured longitudinally at 15-month intervals. Analyses measured the associations between predictor variables and the memory score, and whether AT(N) biomarker profiles significantly improved prediction of memory z score rates of change beyond a model with clinical and genetic variables only. Results: Participants were followed up for a median of 4.8 years (interquartile range [IQR], 3.8-5.1) and 44% were women (211/480). Median (IQR) ages ranged from 67 years (65-73) in the A-T-(N)- group to 83 years (76-87) in the A+T+(N)+ group. Of the participants, 92% (441/480) were cognitively unimpaired but the A+T+(N)+ group had the largest proportion of mild cognitive impairment (30%). AT(N) biomarkers improved the prediction of memory performance over a clinical model from an R2 of 0.26 to 0.31 (P < .001). Memory declined fastest in the A+T+(N)+, A+T+(N)-, and A+T-(N)+ groups compared with the other 5 AT(N) groups (P = .002). Estimated rates of decline in the 3 fastest declining groups were -0.13 (95% CI, -0.17 to -0.09), -0.10 (95% CI, -0.16 to -0.05), and -0.10 (95% CI, -0.13 to -0.06) z score units per year, respectively, for an 85-year-old APOE ε4 noncarrier. Conclusions and Relevance: Among older persons without baseline dementia followed for a median of 4.8 years, a prediction model that included amyloid PET, tau PET, and MRI cortical thickness resulted in a small but statistically significant improvement in predicting memory decline over a model with more readily available clinical and genetic variables. The clinical importance of this difference is uncertain.
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For tau biomarkers, there is a strong discrepancy between neuropathological identification (tau Braak stages I-II almost universal after age 70) and in-vivo measures of tau aggregates on PET (36% of individuals are tau positive after age 70).
“For tau biomarkers, there is also a strong discrepancy between neuropathological identification (in post-mortem studies, the presence of tau Braak stages I–II is almost universal after age 70 years)17,19 and in-vivo measures of tau aggregates on PET (36% of individuals are tau positive after the age of 70 years23).”
From Clinical diagnosis of Alzheimer’s disease: Recommendations of the International Working Group (2021) · cites this paper as [23]
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- Authors
- Jack, C. R., Wiste, H. J., Therneau, T. M., Weigand, S. D., Knopman, D. S., Mielke, M. M., Lowe, V. J., Vemuri, P., Machulda, M. M., Schwarz, C. G., Gunter, J. L., Senjem, M. L., Graff-Radford, J., Jones, D. T., Roberts, R. O., Rocca, W. A., & Petersen, R. C.
- Affiliations
- Mayo Clinic (US)
- Department of Neurology, Mayo Clinic, Rochester, Minnesota
- Corresponding author
- Jack, Clifford R.
- ORCID
- Venue
- JAMA
- Publisher
- American Medical Association (AMA)
- Published
- 2019-06-18
- Volume
- 321
- Issue
- 23
- Pages
- 2316
- ISSN
- 0002-9955 (ISSN-L)
- 0098-7484
- PMC
- PMC6582267
- OpenAlex
- W2951707943
- Cited by
- 324
- References
- 41
- Citations by year
- 2026: 32 · 2025: 47 · 2024: 45 · 2023: 42 · 2022: 51 · 2021: 56 · 2020: 42 · 2019: 9
- FWCI
- 30.96
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- JAMA (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (R01AG034676, U01AG006786, R01AG011378, R01AG041851, R37AG011378, R01AG056366)
- National Institute of Neurological Disorders and Stroke (R01NS097495)
- 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, amyloid PET, tau PET, neurodegeneration biomarkers, memory decline, cognitive aging, mild cognitive impairment, cortical thickness, APOE genotype, prognostic value, Mayo Clinic Study of Aging, older adults without dementia
- MeSH terms
- Aged, Aged, 80 and over, Apolipoproteins E, Brain, Dementia, Female, Genotype, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Cohort Studies, Biomarkers, Amyloid beta-Peptides, tau Proteins, Disease Progression, Positron-Emission Tomography, Cognitive Dysfunction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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