Brain β-amyloid load approaches a plateau
Open accessAbstract
OBJECTIVE: To model the temporal trajectory of β-amyloid accumulation using serial amyloid PET imaging. METHODS: Participants, aged 70-92 years, were enrolled in either the Mayo Clinic Study of Aging (n = 246) or the Mayo Alzheimer's Disease Research Center (n = 14). All underwent 2 or more serial amyloid PET examinations. There were 205 participants classified as cognitively normal and 55 as cognitively impaired (47 mild cognitive impairment and 8 Alzheimer dementia). We measured baseline amyloid PET-relative standardized uptake values (SUVR) and, for each participant, estimated a slope representing their annual amyloid accumulation rate. We then fit regression models to predict the rate of amyloid accumulation given baseline amyloid SUVR, and evaluated age, sex, clinical group, and APOE as covariates. Finally, we integrated the amyloid accumulation rate vs baseline amyloid PET SUVR association to an amyloid PET SUVR vs time association. RESULTS: Rates of amyloid accumulation were low at low baseline SUVR. Rates increased to a maximum at baseline SUVR around 2.0, above which rates declined-reaching zero at baseline SUVR above 2.7. The rate of amyloid accumulation as a function of baseline SUVR had an inverted U shape. Integration produced a sigmoid curve relating amyloid PET SUVR to time. The average estimated time required to travel from an SUVR of 1.5-2.5 is approximately 15 years. CONCLUSION: This roughly 15-year interval where the slope of the amyloid SUVR vs time curve is greatest and roughly linear represents a large therapeutic window for secondary preventive interventions.
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Aβ aggregation begins in preclinical phase of AD; patients may exhibit Aβ plaque pathology for more than a decade before clinical diagnosis.
“Aβ aggregation begins in the preclinical phase of AD. Patients may exhibit Aβ plaque pathology for more than a decade before any clinical diagnosis of AD,29,30”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [30]
The Results section reports amyloid deposition in some cognitively normal participants and describes it as an earlier event than cognitive impairment. It also estimates roughly 15 years of amyloid accumulation between specified PET levels, but does not establish that patients had plaque pathology for more than a decade before an AD diagnosis. (LLM, conf=0.85)
Experimental — accuracy not yet measuredSplines have been used extensively in the literature to model longitudinal changes in Alzheimer disease biomarkers.
“Splines have also been used extensively in the literature to model longitudinal changes in Alzheimer disease biomarkers33,34.”
From Spatial patterns of neuroimaging biomarker change in individuals from families with autosomal dominant Alzheimer's disease: a longitudinal study (2018) · cites this paper as [33]
Plaque formation rates vary over time; after rapid accumulation, plaque deposition gradually slows and by symptom manifestation is essentially done.
“Plaque formation rates also vary over time [217]. After a period of rapid accumulation, plaque deposition gradually slows and by the time symptoms manifest plaque deposition is essentially done [20, 205, 218].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [217]
Plaque deposition essentially occurs during the run-up to clinical AD.
“Recent data indicate plaque deposition essentially occurs during the run-up to clinical AD [216, 217].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [217]
Symptoms generally manifest only after plaques stop forming.
“data argue symptoms generally manifest only after plaques stop forming (Figure 5) [205, 216, 217].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [217]
Brain amyloidosis burns itself out before clinical signs and symptoms emerge.
“We now know from biomarker studies that brain amyloidosis burns itself out before clinical signs and symptoms emerge [217].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [217]
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In vivo imaging reveals sigmoidal growth kinetic of β-amyloid plaques
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When the infectious environment meets the AD brain
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- Authors
- Jack, C. R., Wiste, H. J., Lesnick, T. G., Weigand, S. D., Knopman, D. S., Vemuri, P., Pankratz, V. S., Senjem, M. L., Gunter, J. L., Mielke, M. M., Lowe, V. J., Boeve, B. F., & Petersen, R. C.
- Affiliations
- Mayo Clinic (US)
- ORCID
- Venue
- Neurology
- Published
- 2013-03-05
- Volume
- 80
- Issue
- 10
- Pages
- 890-896
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- PMC
- PMC3653215
- OpenAlex
- W2150481150
- Cited by
- 406
- References
- 41
- Citations by year
- 2026: 32 · 2025: 20 · 2024: 28 · 2023: 27 · 2022: 25 · 2021: 47 · 2020: 40 · 2019: 22 · 2018: 32 · 2017: 31 · 2016: 24 · 2015: 28 · 2014: 31 · 2013: 19
- FWCI
- 24.09
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neurology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Alzheimer's Association
- Eli Lilly and Company (AG024904)
- Pfizer (AG024904)
- Mayo Foundation for Medical Education and Research (AG16574)
- University of Cambridge
- University of Oxford
- National Institutes of Health (AG11378, U01-AG024904, AG024904, R01 AG11378, R01‐AG011378, AG16574, AG011378)
- National Institute on Aging (U01-AG-024904, R01AG11378, P50‐AG16574, U01AG06786, R01AG040042, AG 024904, AG 16574, AG011378, U01AG006786, R01AG011378, AG-11378, R01AG041851, P50AG016574)
- National Cancer Institute
- National Center for Research Resources (C06RR018898)
- Janssen Pharmaceuticals
- 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 › Radiology, Nuclear Medicine and Imaging › Medical Imaging Techniques and Applications
- Keywords
- amyloid-beta deposition, amyloid PET, serial imaging, S-curve, plateaus, Alzheimer's disease, mild cognitive impairment, apolipoprotein E, secondary prevention, therapeutic window, Mayo Clinic Study of Aging
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Brain, Humans, Amyloid beta-Peptides, Positron-Emission Tomography, Cognitive Dysfunction
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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.
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