Brain injury biomarkers are not dependent on β‐amyloid in normal elderly
Open accessAbstract
Objective: The new criteria for preclinical Alzheimer disease (AD) proposed 3 stages: abnormal levels of β‐amyloid (stage 1), stage 1 plus evidence of brain injury (stage 2), and stage 2 plus subtle cognitive changes (stage 3). However, a large group of subjects with normal β‐amyloid biomarkers have evidence of brain injury; we labeled them as the “suspected non‐Alzheimer pathophysiology” (sNAP) group. The characteristics of the sNAP group are poorly understood. Methods: Using the preclinical AD classification, 430 cognitively normal subjects from the Mayo Clinic Study of Aging who underwent brain magnetic resonance (MR), 18 fluorodeoxyglucose (FDG), and Pittsburgh compound B positron emission tomography (PET) were evaluated for FDG PET regional volumetrics, MR regional brain volumetrics, white matter hyperintensity volume, and number of infarcts. We examined cross‐sectional associations across AD preclinical stages, those with all biomarkers normal, and the sNAP group. Results: The sNAP group had a lower proportion (14%) with apolipoprotein E ε4 genotype than the preclinical AD stages 2 + 3. The sNAP group did not show any group differences compared to stages 2 + 3 of the preclinical AD group on measures of FDG PET regional hypometabolism, MR regional brain volume loss, cerebrovascular imaging lesions, vascular risk factors, imaging changes associated with α‐synucleinopathy, or physical findings of parkinsonism. Interpretation: Cognitively normal persons with brain injury biomarker abnormalities, with or without abnormal levels of β‐amyloid, were indistinguishable on a variety of imaging markers, clinical features, and risk factors. The initial appearance of brain injury biomarkers that occurs in cognitively normal persons with preclinical AD may not depend on β‐amyloidosis. ANN NEUROL 2013;73:472–480
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The rate of cognitive decline is significantly greater for cognitively impaired and CU individuals who have abnormalities in both an amyloid biomarker and a second biomarker type (CSF T-tau or P-tau, atrophy, or hypometabolism) in comparison to individuals who have neither or only one of these biomarker abnormalities.
“The rate of cognitive decline is significantly greater for cognitively impaired and CU individuals who have abnormalities in both an amyloid biomarker and a second biomarker type (which could be CSF T-tau or P-tau, atrophy, or hypometabolism) in comparison to individuals who have neither or only one of these biomarker abnormalities [30–35,39,40,42–45].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [30]
The Introduction (page unavailable) reports that cognitively normal participants with both amyloid and brain-injury abnormalities had a higher one-year risk of cognitive decline than groups with only one abnormality. It does not establish the claimed significant difference in rates across cognitively impaired and cognitively unimpaired people; this study examined cognitively normal participants and used atrophy or hypometabolism, not CSF tau, as its brain-injury biomarkers. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe combination of an abnormal MRI, CSF T-tau, or FDG PET study with an abnormal amyloid biomarker provides much more powerful prediction of future cognitive decline than an abnormal amyloid study alone.
“However, the combination of an abnormal MRI, CSF T-tau, or FDG PET study with an abnormal amyloid biomarker provides much more powerful prediction of future cognitive decline [30–35,39,40,42–45] than an abnormal amyloid study alone.”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [30]
The Introduction (page unavailable) reports that cognitively normal participants with amyloid and brain-injury biomarker abnormalities (preclinical stages 2–3) had more than twice the one-year risk of cognitive decline of those with abnormal amyloid alone (stage 1). The paper uses MRI and FDG PET as brain-injury markers, but not CSF T-tau; its own analysis is cross-sectional rather than a direct test of future prediction. (LLM, conf=0.85)
Experimental — accuracy not yet measuredFor many subjects with suspected AD or increased risk, what are currently considered downstream biomarker changes potentially precede upstream biomarker changes.
“Our hypothesis, therefore, can accommodate a growing realization that for many subjects with suspected AD, or who have an increased risk of developing AD, what are currently considered downstream biomarker changes potentially precede upstream biomarker changes [206-213].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [206]
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Zetterberg, H., & Mattsson, N. (2014) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.2014.915740 · Cited by 73 · see citing works
Knopman, D. S., Jack, C. R., Wiste, H. J., Weigand, S. D., Vemuri, P., Lowe, V. J., Kantarci, K., Gunter, J. L., Senjem, M. L., Mielke, M. M., et al. (2013) · JAMA Neurology · doi:10.1001/jamaneurol.2013.182 · Cited by 68 · see citing works
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Tracking the earliest pathologic changes in Alzheimer disease
Landau, S. M., & Frosch, M. P. (2014) · Neurology · doi:10.1212/wnl.0000000000000392 · Cited by 20 · see citing works
- Authors
- Knopman, D. S., Jack, C. R., Wiste, H. J., Weigand, S. D., Vemuri, P., Lowe, V. J., Kantarci, K., Gunter, J. L., Senjem, M. L., Mielke, M. M., Roberts, R. O., Boeve, B. F., & Petersen, R. C.
- Affiliations
- Mayo Clinic (US)
- Corresponding author
- Knopman, David S.
- ORCID
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2013-02-19
- Volume
- 73
- Issue
- 4
- Pages
- 472-480
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- PMC
- PMC3660408
- OpenAlex
- W1948376220
- Cited by
- 183
- References
- 49
- Citations by year
- 2026: 1 · 2025: 5 · 2024: 7 · 2023: 3 · 2022: 10 · 2021: 12 · 2020: 6 · 2019: 12 · 2018: 16 · 2017: 20 · 2016: 19 · 2015: 22 · 2014: 33 · 2013: 17
- FWCI
- 16.39
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG11378, P50‐AG16574, U01AG06786, U01AG006786, R01AG011378, R01 AG41851, R01AG041851, P50AG016574)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- preclinical Alzheimer's disease, brain injury biomarkers, amyloid-beta, cognitively normal elderly, APOE ε4, FDG-PET hypometabolism, brain atrophy, white matter hyperintensities, cerebral infarction, cerebrovascular risk factors, synucleinopathies, parkinsonism, Mayo Clinic Study of Aging
- MeSH terms
- Aged, Aged, 80 and over, Brain, Cerebral Cortex, Cerebrovascular Disorders, Female, Humans, Male, Risk Factors, Biomarkers, Fluorodeoxyglucose F18, Positron-Emission Tomography, Synucleins
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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.
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