Accuracy of Brain Amyloid Detection in Clinical Practice Using Cerebrospinal Fluid β-Amyloid 42: A Cross-Validation Study Against Amyloid Positron Emission Tomography
Abstract
IMPORTANCE: Before adding cerebrospinal fluid (CSF) biomarkers to the diagnostic workup of Alzheimer disease, it needs to be determined whether CSF biomarkers analyzed in routine clinical practice can reliably predict cortical β-amyloid (Aβ) deposition. OBJECTIVES: To study whether CSF biomarkers, analyzed consecutively in routine clinical practice during 2 years, can predict cortical Aβ deposition and to establish a threshold for Aβ42 abnormality. DESIGN, SETTING, AND PARTICIPANTS: This cross-sectional study (The Swedish BioFINDER [Biomarkers For Identifying Neurodegenerative Disorders Early and Reliably] Study) was conducted at 3 memory clinics. It involved consecutively referred, nondemented patients with mild cognitive symptoms (original cohort, n = 118; validation cohort, n = 38). EXPOSURES: Amyloid positron emission tomography imaging with 18F-flutemetamol. MAIN OUTCOMES AND MEASURES: Analyses of CSF Aβ42, total tau, and phosphorylated tau using an enzyme-linked immunosorbent assay (INNOTEST) in clinical samples. RESULTS: The agreement between Aβ classification with CSF Aβ42 and 18F-flutemetamol positron emission tomography was very high (κ = 0.85). Of all the cases, 92% were classified identically using an Aβ42 cutoff of 647 pg/mL or less. Cerebrospinal fluid Aβ42 predicted abnormal cortical Aβ deposition accurately (odds ratio, 165; 95% CI, 39-693; area under the receiver operating characteristic curve, 0.94; 95% CI, 0.88-0.97). The association was independent of age, sex, APOE (apolipoprotein E) genotype, hippocampal volume, memory, and global cognition (adjusted odds ratio, 169; 95% CI, 25-1143). Using ratios of CSF Aβ42:tau or Aβ42:phosphorylated tau did not improve the prediction of Aβ deposition. Cerebrospinal fluid Aβ42 correlated significantly with Aβ deposition in all cortical regions. The highest correlations were in regions with high 18F-flutemetamol retention (eg, posterior cingulum and precuneus, r = -0.72). 18F-flutemetamol retention, but not CSF Aβ42, correlated significantly with global cognition (r = -0.32), memory function (r = -0.28), and hippocampal volume (r = -0.36) among those with abnormal Aβ deposition. Finally, the CSF Aβ42 cutoff derived from the original cohort (≤647 pg/mL) had an equally high agreement (95%; κ = 0.89) with 18F-flutemetamol positron emission tomography in the validation cohort. CONCLUSIONS AND RELEVANCE: Cerebrospinal fluid Aβ42 analyzed consecutively in routine clinical practice at an accredited laboratory can be used with high accuracy to determine whether a patient has normal or increased cortical Aβ deposition and so can be valuable for the early diagnosis of Alzheimer disease. Abnormal 18F-flutemetamol retention levels correlate with disease stage in patients with mild cognitive symptoms, but this is not the case for CSF Aβ42 measurements.
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Mixture modeling provides an unbiased threshold for abnormality and is a well-established method for defining Aβ PET cut-offs.
“Mixture modeling statistics provide an unbiased threshold for abnormality (i.e., the diagnosis or status is not used in analysis) and it is a well-established method for defining Aβ PET cut-offs12, 17, 60, 61.”
From Earliest accumulation of β-amyloid occurs within the default-mode network and concurrently affects brain connectivity (2017) · cites this paper as [60]
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Self-citationA Review of Fluid Biomarkers for Alzheimer’s Disease: Moving from CSF to Blood
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Self-citationMultiplex proteomics identifies novel CSF and plasma biomarkers of early Alzheimer’s disease
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Self-citationAssociation of Amyloid Pathology With Myelin Alteration in Preclinical Alzheimer Disease
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Self-citationAdvances in the development of new biomarkers for Alzheimer’s disease
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Self-citationStaging <b>β</b> -Amyloid Pathology With Amyloid Positron Emission Tomography
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Self-citationCerebrospinal fluid tau and amyloid-β1-42in patients with dementia
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Self-citationCerebrospinal Fluid Patterns and the Risk of Future Dementia in Early, Incident Parkinson Disease
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Self-citationCentiloid cut-off values for optimal agreement between PET and CSF core AD biomarkers
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Self-citationValidation of Plasma Amyloid-β 42/40 for Detecting Alzheimer Disease Amyloid Plaques
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Self-citationAmyloid blood biomarker detects Alzheimer's disease
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Self-citationApathy and anxiety are early markers of Alzheimer's disease.
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Self-citation18F‐AV‐1451 and CSF T‐tau and P‐tau as biomarkers in Alzheimer's disease
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Self-citationPatient-centered connectivity-based prediction of tau pathology spread in Alzheimer’s disease
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Self-citationAn accurate fully automated panel of plasma biomarkers for Alzheimer's disease
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Self-citationClinical effects of Lewy body pathology in cognitively impaired individuals
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Self-citationCerebrospinal fluid biomarkers in trials for Alzheimer and Parkinson diseases
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Self-citationThe Past and the Future of Alzheimer’s Disease Fluid Biomarkers
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Self-citationPlasma Amyloid-β (Aβ 42 ) Correlates with Cerebrospinal Fluid Aβ 42 in Alzheimer’s Disease
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Self-citationPlasma markers predict changes in amyloid, tau, atrophy and cognition in non-demented subjects
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Self-citationDetermining clinically meaningful decline in preclinical Alzheimer disease
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Self-citationAlzheimer's disease cerebrospinal fluid biomarker in cognitively normal subjects
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Self-citationNeurogranin, a synaptic protein, is associated with memory independent of Alzheimer biomarkers
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Self-citationCerebrospinal Fluid Biomarkers of Neurovascular Dysfunction in Mild Dementia and Alzheimer'S Disease
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In vivo retention of <sup>18</sup> F-AV-1451 in corticobasal syndrome
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The implications of different approaches to define AT(N) in Alzheimer disease
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Increased midlife triglycerides predict brain β-amyloid and tau pathology 20 years later
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Association of Enlarged Perivascular Spaces and Measures of Small Vessel and Alzheimer Disease
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Self-citationFluid and PET biomarkers for amyloid pathology in Alzheimer's disease
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Self-citationEffects of acute sleep loss on diurnal plasma dynamics of CNS health biomarkers in young men
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Self-citationComparing 18 F-AV-1451 with CSF t-tau and p-tau for diagnosis of Alzheimer disease
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Self-citationDetecting earlier stages of amyloid deposition using PET in cognitively normal elderly adults
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Self-citationCurrent advances in plasma and cerebrospinal fluid biomarkers in Alzheimer's disease
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Self-citationUnbiased estimates of cerebrospinal fluid β-amyloid 1–42 cutoffs in a large memory clinic population
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Self-citationAlzheimer’s Disease Biomarkers and Future Decline in Cognitive Normal Older Adults
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Molecular imaging in dementia: Past, present, and future
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Self-citationMidlife Atherosclerosis and Development of Alzheimer or Vascular Dementia
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Self-citation
- Authors
- Palmqvist, S., Zetterberg, H., Blennow, K., Vestberg, S., Andreasson, U., Brooks, D. J., Owenius, R., Hägerström, D., Wollmer, P., Minthon, L., & Hansson, O.
- Affiliations
- Lund University (SE)
- University of Gothenburg (SE)
- Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg and Mölndal, Sweden
- Aarhus University (DK)
- GE Healthcare, Life Sciences, Uppsala, Sweden
- Skåne University Hospital (SE)
- Corresponding author
- Hansson, Oskar
- ORCID
- Venue
- JAMA Neurology
- Publisher
- American Medical Association (AMA)
- Published
- 2014-10-01
- Volume
- 71
- Issue
- 10
- Pages
- 1282
- ISSN
- 2168-6149 (ISSN-L)
- OpenAlex
- W1992165389
- Cited by
- 368
- References
- 48
- Citations by year
- 2026: 5 · 2025: 25 · 2024: 21 · 2023: 16 · 2022: 27 · 2021: 38 · 2020: 48 · 2019: 46 · 2018: 31 · 2017: 34 · 2016: 33 · 2015: 39 · 2014: 3
- FWCI
- 27.74
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- JAMA Neurology (publishedVersion)
- PubMed (publishedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- 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 › Cellular and Molecular Neuroscience › Cerebrospinal fluid and hydrocephalus
- Keywords
- Alzheimer's disease, cerebrospinal fluid biomarkers, amyloid-beta 42, cortical amyloid deposition, 18F-flutemetamol PET, total tau, phosphorylated tau, diagnostic accuracy, mild cognitive impairment, APOE genotype, hippocampal volume, memory clinics, early detection of neurodegeneration
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Aniline Compounds, Brain, Cerebral Cortex, Cross-Sectional Studies, Female, Gyrus Cinguli, Humans, Male, Middle Aged, Peptide Fragments, Reproducibility of Results, Cohort Studies, Amyloid beta-Peptides, Radiopharmaceuticals, Early Diagnosis, Positron-Emission Tomography, Benzothiazoles, 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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