Predicting future rates of tau accumulation on PET
Open accessAbstract
Clinical trials with anti-tau drugs will need to target individuals at risk of accumulating tau. Our objective was to identify variables available in a research setting that predict future rates of tau PET accumulation separately among individuals who were either cognitively unimpaired or cognitively impaired. All 337 participants had: a baseline study visit with MRI, amyloid PET, and tau PET exams, at least one follow-up tau PET exam; and met clinical criteria for membership in one of two clinical diagnostic groups: cognitively unimpaired (n = 203); or cognitively impaired (n = 134, a combined group of participants with either mild cognitive impairment or dementia with Alzheimer’s clinical syndrome). Our primary analyses were in these two clinical groups; however, we also evaluated subgroups dividing the unimpaired group by normal/abnormal amyloid PET and the impaired group by clinical phenotype (mild cognitive impairment, amnestic dementia, and non-amnestic dementia). Linear mixed effects models were used to estimate associations between age, sex, education, APOE genotype, amyloid and tau PET standardized uptake value ratio (SUVR), cognitive performance, cortical thickness, and white matter hyperintensity volume at baseline, and the rate of subsequent tau PET accumulation. Log-transformed tau PET SUVR was used as the response and rates were summarized as annual per cent change. A temporal lobe tau PET meta-region of interest was used. In the cognitively unimpaired group, only higher baseline amyloid PET was a significant independent predictor of higher tau accumulation rates (P < 0.001). Higher rates of tau accumulation were associated with faster rates of cognitive decline in the cognitively unimpaired subgroup with abnormal amyloid PET (P = 0.03), but among the subgroup with normal amyloid PET. In the cognitively impaired group, younger age (P = 0.02), higher baseline amyloid PET (P = 0.05), APOE ε4 (P = 0.05), and better cognitive performance (P = 0.05) were significant independent predictors of higher tau accumulation rates. Among impaired individuals, faster cognitive decline was associated with faster rates of tau accumulation (P = 0.01). While we examined many possible predictor variables, our results indicate that screening of unimpaired individuals for potential inclusion in anti-tau trials may be straightforward because the only independent predictor of high tau rates was amyloidosis. In cognitively impaired individuals, imaging and clinical variables consistent with early onset Alzheimer’s disease phenotype were associated with higher rates of tau PET accumulation suggesting this may be a highly advantageous group in which to conduct proof-of-concept clinical trials that target tau-related mechanisms. The nature of the dementia phenotype (amnestic versus non-amnestic) did not affect this conclusion.
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A level of 20 centiloids or less is an accepted threshold for amyloid negativity.
“From this work, ≤20 CL is an accepted threshold for amyloid negativity.”
From The amyloid hypothesis in Alzheimer disease: new insights from new therapeutics (2022) · cites this paper as [88]
Amadoru et al. found the optimum threshold between low and high amyloid plaque was 21 CL, and 10 CL for none versus any.
“The optimum threshold between low vs high amyloid plaque was 21 CL; and 10 CL for none vs. any.”
From The amyloid hypothesis in Alzheimer disease: new insights from new therapeutics (2022) · cites this paper as [88]
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Jack, C. R., Wiste, H. J., Botha, H., Weigand, S. D., Therneau, T. M., Knopman, D. S., Graff-Radford, J., Jones, D. T., Ferman, T. J., Boeve, B. F., et al. (2019) · Brain · doi:10.1093/brain/awz268 · Cited by 200 · see citing works
Self-citationDementia and Alzheimer Disease Incidence Rates Do Not Vary by Sex in Rochester, Minn
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Self-citationDistinct 18F-AV-1451 tau PET retention patterns in early- and late-onset Alzheimer’s disease
Schöll, M., Ossenkoppele, R., Strandberg, O., Palmqvist, S., study, T. S. B., Jögi, J., Ohlsson, T., Smith, R., & Hansson, O. (2017) · Brain · doi:10.1093/brain/awx171 · Cited by 180 · see citing works
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Self-citationAV-1451 PET imaging of tau pathology in preclinical Alzheimer disease: Defining a summary measure
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Indicators of amyloid burden in a population-based study of cognitively normal elderly
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Self-citationAssociation of Cerebral Amyloid-β Aggregation With Cognitive Functioning in Persons Without Dementia
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Distinct tau PET patterns in atrophy‐defined subtypes of Alzheimer's disease
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FDG-PET in tau-negative amnestic dementia resembles that of autopsy-proven hippocampal sclerosis
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Entorhinal cortex tau, amyloid-β, cortical thickness and memory performance in non-demented subjects
Knopman, D. S., Lundt, E. S., Therneau, T. M., Vemuri, P., Lowe, V. J., Kantarci, K., Gunter, J. L., Senjem, M. L., Mielke, M. M., Machulda, M. M., et al. (2019) · Brain · doi:10.1093/brain/awz025 · Cited by 100 · see citing works
Self-citationAmyloid duration is associated with preclinical cognitive decline and tau PET
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Progressive Tau Accumulation in Alzheimer Disease: 2-Year Follow-up Study
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Self-citationGordon, B. A., McCullough, A. A., Mishra, S., Blazey, T., Su, Y., Christensen, J., Dincer, A., Jackson, K., Hornbeck, R. C., Morris, J. C., et al. (2018) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1016/j.dadm.2018.02.003 · Cited by 86 · see citing works
A Comparison of Partial Volume Correction Techniques for Measuring Change in Serial Amyloid PET SUVR
Schwarz, C. G., Gunter, J. L., Lowe, V. J., Weigand, S. D., Vemuri, P., Senjem, M. L., Petersen, R. C., Knopman, D. S., & Jack, C. R. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180749 · Cited by 85 · see citing works
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Longitudinal tau-PET uptake and atrophy in atypical Alzheimer's disease
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Self-citationSuspected non-AD pathology in mild cognitive impairment
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Anti-Tau Trials for Alzheimer's Disease: A Report from the EU/US/CTAD Task Force
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Age at onset is associated with disease severity in Lewy body variant and Alzheimer's disease
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Brain structure and function as mediators of the effects of amyloid on memory
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Self-citationAmyloid Imaging in Dementias With Atypical Presentation
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Self-citationTau-negative amnestic dementia masquerading as Alzheimer disease dementia
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Biomarkers for neurodegenerative diseases
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The amyloid hypothesis in Alzheimer disease: new insights from new therapeutics
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- Authors
- Jack, C. R., Wiste, H. J., Weigand, S. D., Therneau, T. M., Lowe, V. J., Knopman, D. S., Botha, H., Graff-Radford, J., Jones, D. T., Ferman, T. J., Boeve, B. F., Kantarci, K., Vemuri, P., Mielke, M. M., Whitwell, J., Josephs, K., Schwarz, C. G., Senjem, M. L., Gunter, J. L., & Petersen, R. C.
- Affiliations
- Mayo Clinic (US)
- Department of Neurology, Mayo Clinic, Rochester, MN, USA
- Corresponding author
- Jack, Clifford R
- ORCID
- Jack, Clifford R
- Wiste, Heather J
- Weigand, Stephen D
- Therneau, Terry M
- Lowe, Val J
- Knopman, David S
- Botha, Hugo
- Graff-Radford, Jonathan
- Jones, David T
- Ferman, Tanis J
- Boeve, Bradley F
- Kantarci, Kejal
- Vemuri, Prashanthi
- Mielke, Michelle M
- Whitwell, Jennifer
- Josephs, Keith
- Schwarz, Christopher G
- Senjem, Matthew L
- Gunter, Jeffrey L
- Petersen, Ronald C
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2020-06-24
- Volume
- 143
- Issue
- 10
- Pages
- 3136-3150
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC7586089
- OpenAlex
- W3094551933
- Cited by
- 117
- References
- 99
- Citations by year
- 2026: 13 · 2025: 15 · 2024: 12 · 2023: 23 · 2022: 28 · 2021: 24 · 2020: 2
- FWCI
- 14.05
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Brain (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (R01-AG50603, R37 AG011378, RO1 AG041851, R01 AG056366, R01 NS097495, U01 AG06786, R01 AG034676, P50 AG016574)
- Alexander Family Professorship of Alzheimer’s Disease Research
- Robert Wood Johnson Foundation
- The Elsie and Marvin Dekelboum Family Foundation
- The Liston Family Foundation
- GHR Foundation
- Foundation Dr. Corinne Schuler
- Alzheimer’s Association
- Mayo Foundation
- 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
- tau accumulation, amyloid PET, amyloidosis, Alzheimer's disease, cognitive decline, mild cognitive impairment, dementia, APOE ε4, temporal lobe, white matter hyperintensities, cortical thickness, standardized uptake value ratio, risk prediction
- MeSH terms
- Aged, Aged, 80 and over, Female, Forecasting, Humans, Longitudinal Studies, Male, Middle Aged, Predictive Value of Tests, Cohort Studies, tau Proteins, 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.
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