The relationship between cerebrospinal fluid markers of Alzheimer pathology and positron emission tomography tau imaging
Open accessAbstract
The two primary molecular pathologies in Alzheimer's disease are amyloid-β plaques and tau-immunoreactive neurofibrillary tangles. Investigations into these pathologies have been restricted to cerebrospinal fluid assays, and positron emission tomography tracers that can image amyloid-β plaques. Tau tracers have recently been introduced into the field, although the utility of the tracer and its relationship to other Alzheimer biomarkers are still unknown. Here we examined tau deposition in 41 cognitively normal and 11 cognitively impaired older adults using the radioactive tau ligand (18)F-AV-1451 (previously known as T807) who also underwent a lumbar puncture to assess cerebrospinal fluid levels of total tau (t-tau), phosphorylated tau181 (p-tau181) and amyloid-β42 Voxel-wise statistical analyses examined spatial patterns of tau deposition associated with cognitive impairment. We then related the amount of tau tracer uptake to levels of cerebrospinal fluid biomarkers. All analyses controlled for age and gender and, when appropriate, the time between imaging and lumbar puncture assessments. Symptomatic individuals (Clinical Dementia Rating > 0) demonstrated markedly increased levels of tau tracer uptake. This elevation was most prominent in the temporal lobe and temporoparietal junction, but extended more broadly into parietal and frontal cortices. In the entire cohort, there were significant relationships among all cerebrospinal fluid biomarkers and tracer uptake, notably for tau-related cerebrospinal fluid markers. After controlling for levels of amyloid-β42, the correlations with tau uptake were r = 0.490 (P < 0.001) for t-tau and r = 0.492 (P < 0.001) for p-tau181 Within the cognitively normal cohort, levels of amyloid-β42, but not t-tau or p-tau181, were associated with elevated tracer binding that was confined primarily to the medial temporal lobe and adjacent neocortical regions. AV-1451 tau binding in the medial temporal, parietal, and frontal cortices is correlated with tau-related cerebrospinal fluid measures. In preclinical Alzheimer's disease, there is focal tauopathy in the medial temporal lobes and adjacent cortices.
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CSF biomarkers are measures of the concentrations of proteins in CSF from the lumbar sac that reflect the rates of both production and clearance at a given point in time.
“CSF biomarkers are measures of the concentrations of proteins in CSF from the lumbar sac that reflect the rates of both production (protein expression or release/secretion from neurons or other brain cells) and clearance (degradation or removal) at a given point in time [114,115].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [115]
The CSF assessment section (page unavailable in our copy) reports that CSF samples were collected and concentrations of tau, phosphorylated tau, and amyloid-β42 were measured in pg/ml; the Participants section says CSF was obtained by lumbar puncture. Neither section, nor the passages retrieved for production and clearance, says those concentrations reflect the rates of protein production and clearance at a given point in time. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe correlation between tau PET ligand binding and elevated CSF P-tau is imperfect.
“In the limited data currently available, tau PET ligand binding is linearly correlated with elevated CSF P-tau [82,83,115]; however, the correlation is imperfect.”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [115]
In the limited data currently available, tau PET ligand binding is linearly correlated with elevated CSF P-tau.
“In the limited data currently available, tau PET ligand binding is linearly correlated with elevated CSF P-tau [82,83,115]; however, the correlation is imperfect.”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [115]
Differences among (N) biomarkers may result in discordances.
“These differences may result in discordances [36,43,115,119,159].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [115]
The correlation between CSF T-tau and P-tau is typically much higher than between CSF T-tau and MRI measures of atrophy or FDG PET.
“CSF levels of T-tau and P-tau are tightly correlated within cohorts of AD patients and controls [145], and the correlation between CSF T-tau and P-tau is typically much higher than between CSF T-tau and MRI measures of atrophy or FDG PET [36,115].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [115]
The ‘Relationship among PET tau binding and CSF biomarkers’ section reports separate correlations of CSF T-tau and P-tau with tau PET, not a correlation between the two CSF measures. The Discussion proposes future analyses using metabolism and structural atrophy; our copy does not compare the claimed correlations with MRI atrophy or FDG PET (searched: T-tau/P-tau correlation, MRI atrophy, FDG PET). Page numbers were unavailable in the indexed passages. (LLM, conf=0.76)
Experimental — accuracy not yet measured
The sensitivity and specificity of Tau PET and CSF P-tau to identify abnormalities in tau metabolism differ.
“Our current results, together with previous findings (14), suggest that the sensitivity and specificity of Tau PET and CSF P-tau to identify abnormalities in tau metabolism differ.”
From Aβ deposition is associated with increases in soluble and phosphorylated tau that precede a positive tau PET in Alzheimer's disease (2020) · cites this paper as [14]
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Self-citationAlzheimer's drug‐development pipeline: 2016
Cummings, J., Morstorf, T., & Lee, G. (2016) · Alzheimer's & Dementia: Translational Research & Clinical Interventions · doi:10.1016/j.trci.2016.07.001 · Cited by 108 · see citing works
Wisch, J. K., McKay, N. S., Boerwinkle, A. H., Kennedy, J., Flores, S., Handen, B. L., Christian, B. T., Head, E., Mapstone, M., Rafii, M. S., et al. (2024) · The Lancet Neurology · doi:10.1016/s1474-4422(24)00084-x · Cited by 37 · see citing works
Self-citationIn vivo [ <sup>18</sup> F]-AV-1451 tau-PET imaging in sporadic Creutzfeldt-Jakob disease
Day, G. S., Gordon, B. A., Perrin, R. J., Cairns, N. J., Beaumont, H., Schwetye, K., Ferguson, C., Sinha, N., Bucelli, R., Musiek, E. S., et al. (2018) · Neurology · doi:10.1212/wnl.0000000000005064 · Cited by 26 · see citing works
Self-citationProteomic clusters underlie heterogeneity in preclinical Alzheimer’s disease progression
Wisch, J. K., Butt, O. H., Gordon, B. A., Schindler, S. E., Fagan, A. M., Henson, R. L., Yang, C., Boerwinkle, A. H., Benzinger, T. L. S., Holtzman, D. M., et al. (2023) · Brain · doi:10.1093/brain/awac484 · Cited by 11 · see citing works
Self-citation
- Authors
- Gordon, B. A., Friedrichsen, K., Brier, M., Blazey, T., Su, Y., Christensen, J., Aldea, P., McConathy, J., Holtzman, D. M., Cairns, N. J., Morris, J. C., Fagan, A. M., Ances, B. M., & Benzinger, T. L. S.
- Affiliations
- Washington University in St. Louis (US)
- ORCID
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2016-06-10
- Volume
- 139
- Issue
- 8
- Pages
- 2249-2260
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC4958902
- OpenAlex
- W2412942072
- Cited by
- 184
- References
- 48
- Citations by year
- 2026: 5 · 2025: 11 · 2024: 11 · 2023: 10 · 2022: 13 · 2021: 24 · 2020: 27 · 2019: 20 · 2018: 27 · 2017: 25 · 2016: 10
- FWCI
- 24.29
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Brain (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- Foundation for Barnes-Jewish Hospital
- Hope Center for Neurological Disorders
- Foundation of Hope for Research and Treatment of Mental Illness
- National Institutes of Health (UL1TR000448)
- National Institute on Aging (P50AG005681, P01AG003991, P01AG026276)
- National Institute of Neurological Disorders and Stroke (P30NS048056)
- National Center for Advancing Translational Sciences
- 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, tau PET imaging, cerebrospinal fluid biomarkers, total tau, phosphorylated tau 181, amyloid-beta 42, tau deposition, preclinical Alzheimer's disease, cognitive impairment, medial temporal lobe, tauopathy, amyloid plaques
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Carbolines, Female, Humans, Male, Peptide Fragments, Biomarkers, Amyloid beta-Peptides, tau Proteins, Positron-Emission Tomography
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