Tau PET in autosomal dominant Alzheimer's disease: relationship with cognition, dementia and other biomarkers
Open accessAbstract
Tauopathy is a hallmark pathology of Alzheimer's disease with a strong relationship with cognitive impairment. As such, understanding tau may be a key to clinical interventions. In vivo tauopathy has been measured using cerebrospinal fluid assays, but these do not provide information about where pathology is in the brain. The introduction of PET ligands that bind to paired helical filaments provides the ability to measure the amount and distribution of tau pathology. The heritability of the age of dementia onset tied to the specific mutations found in autosomal dominant Alzheimer's disease families provides an elegant model to study the spread of tau across the course of the disease as well as the cross-modal relationship between tau and other biomarkers. To better understand the pathobiology of Alzheimer's disease we measured levels of tau PET binding in individuals with dominantly inherited Alzheimer's disease using data from the Dominantly Inherited Alzheimer Network (DIAN). We examined cross-sectional measures of amyloid-β, tau, glucose metabolism, and grey matter degeneration in 15 cognitively normal mutation non-carriers, 20 asymptomatic carriers, and 15 symptomatic mutation carriers. Linear models examined the association of pathology with group, estimated years to symptom onset, as well as cross-modal relationships. For comparison, tau PET was acquired on 17 older adults with sporadic, late onset Alzheimer disease. Tau PET binding was starkly elevated in symptomatic DIAN individuals throughout the cortex. The brain areas demonstrating elevated tau PET binding overlapped with those seen in sporadic Alzheimer's disease, but with a greater cortical involvement and greater levels of binding despite similar cognitive impairment. Tau PET binding was elevated in the temporal lobe, but the most prominent loci of pathology were in the precuneus and lateral parietal regions. Symptomatic mutation carriers also demonstrated elevated tau PET binding in the basal ganglia, consistent with prior work with amyloid-β. The degree of tau tracer binding in symptomatic individuals was correlated to other biomarkers, particularly markers of neurodegeneration. In addition to the differences seen with tau, amyloid-β was increased in both asymptomatic and symptomatic groups relative to non-carriers. Glucose metabolism showed decline primarily in the symptomatic group. MRI indicated structural degeneration in both asymptomatic and symptomatic cohorts. We demonstrate that tau PET binding is elevated in symptomatic individuals with dominantly inherited Alzheimer's disease. Tau PET uptake was tied to the onset of cognitive dysfunction, and there was a higher amount, and different regional pattern of binding compared to late onset, non-familial Alzheimer's disease.
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Tau PET uptake occurs at a later stage and age than amyloid PET and is more closely associated with cognitive dysfunction than amyloid-PET.
“Tau PET uptake occurs at a later stage and age than amyloid Pet and is more closely associated with cognitive dysfunction than amyloid-PET.(442, 443)”
From Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission (2024) · cites this paper as [442]
In the Group-wise comparisons within ADAD section, amyloid PET binding is elevated in asymptomatic mutation carriers, whereas tau PET binding is significantly elevated only in symptomatic carriers. The Discussion links this later tau PET increase to cognitive impairment, but the paper does not establish a precise age of tau uptake or directly show that its association with cognitive dysfunction is stronger than amyloid PET’s. Its findings also concern primarily autosomal dominant Alzheimer’s disease, rather than Alzheimer’s disease generally. (LLM, conf=0.84)
Experimental — accuracy not yet measuredIncreases in CSF p-tau occur before both tau PET and established measures of neuronal death, so CSF p-tau cannot merely reflect NFT leakage from dying neurons.
“Increases in CSF p-tau occur before both tau PET20,63,64 and established measures of neuronal death (e.g., neurofilament light, magnetic resonance imaging or [18F]FDG PET), thus CSF p-tau cannot merely reflect NFT leakage from dying neurons.”
From Cerebrospinal fluid p-tau231 as an early indicator of emerging pathology in Alzheimer's disease (2022) · cites this paper as [64]
The Discussion says CSF measures of tauopathy likely become abnormal before tau PET measures, supporting the timing comparison to which this citation is attached. It also says the timing results are qualitative and that larger studies are needed to establish the order definitively; the citing sentence states that order as fact. (LLM, conf=0.86)
Experimental — accuracy not yet measured
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Self-citationWidespread distribution of tauopathy in preclinical Alzheimer's disease
Schultz, S. A., Gordon, B. A., Mishra, S., Su, Y., Perrin, R. J., Cairns, N. J., Morris, J. C., Ances, B. M., & Benzinger, T. L. S. (2018) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2018.08.022 · Cited by 63 · see citing works
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Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission
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Self-citationCSF tau microtubule binding region identifies tau tangle and clinical stages of Alzheimer’s disease
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Self-citation
- Authors
- Gordon, B. A., Blazey, T. M., Christensen, J., Dincer, A., Flores, S., Keefe, S., Chen, C., Su, Y., McDade, E. M., Wang, G., Li, Y., Hassenstab, J., Aschenbrenner, A., Hornbeck, R., Jack, C. R., Ances, B. M., Berman, S. B., Brosch, J. R., Galasko, D., Gauthier, S., Lah, J. J., Masellis, M., van Dyck, C. H., Mintun, M. A., Klein, G., Ristic, S., Cairns, N. J., Marcus, D. S., Xiong, C., Holtzman, D. M., Raichle, M. E., Morris, J. C., Bateman, R. J., & Benzinger, T. L. S.
- Affiliations
- Washington University in St. Louis (US)
- Banner Health (US)
- Mayo Clinic (US)
- University of Pittsburgh (US)
- Indiana University Indianapolis (US)
- University of California San Diego (US)
- McGill University (CA)
- Emory University (US)
- Sunnybrook Health Science Centre (CA)
- Alzheimer’s Disease Research Unit, Yale University School of Medicine, New Haven, CT, USA
- Avid Radiopharmaceuticals (United States) (US)
- F. Hoffmann-La Roche AG (CH)
- Corresponding author
- Gordon, Brian A
- ORCID
- Gordon, Brian A
- Blazey, Tyler M
- Dincer, Aylin
- Flores, Shaney
- Keefe, Sarah
- Chen, Charles
- Su, Yi
- McDade, Eric M
- Wang, Guoqiao
- Li, Yan
- Hassenstab, Jason
- Aschenbrenner, Andrew
- Hornbeck, Russ
- Jack, Clifford R
- Ances, Beau M
- Berman, Sarah B
- Brosch, Jared R
- Galasko, Douglas
- Gauthier, Serge
- Lah, James J
- Masellis, Mario
- Klein, Gregory
- Marcus, Daniel S
- Xiong, Chengjie
- Holtzman, David M
- Raichle, Marcus E
- Morris, John C
- Bateman, Randall J
- Benzinger, Tammie L S
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2019-02-11
- Volume
- 142
- Issue
- 4
- Pages
- 1063-1076
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC6439328
- OpenAlex
- W2913321668
- Cited by
- 180
- References
- 71
- Citations by year
- 2026: 15 · 2025: 22 · 2024: 18 · 2023: 26 · 2022: 24 · 2021: 40 · 2020: 24 · 2019: 10 · 2018: 1
- FWCI
- 16.80
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Brain (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- NIH (K01AG053474, R01AG052550, UFAG 032438, UL1TR000448, P30NS098577, R01EB009352, P50AG05131, U01AG042791, U01AG042791-S1, 1S10RR022984–01A1, 1S10OD018091–01)
- FNIH and Accelerating Medicines Partnership (R1AG046179)
- German Center for Neurodegenerative Diseases
- DZNE
- National Institute for Health Research
- NIHR
- Queen Square Dementia Biomedical Research Centre
- Medical Research Council Dementias Platform UK (MR/L023784/1, MR/009076/1)
- the Alzheimer’s Association
- Eli Lilly and Company
- Genentech/Roche
- Avid Radiopharmaceuticals
- DIAN-TU Pharma Consortium
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
- Keywords
- tau PET, autosomal dominant Alzheimer's disease, tauopathy, paired helical filaments, DIAN, amyloid-beta, glucose metabolism, neurodegeneration biomarkers, dementia onset, basal ganglia, precuneus, temporal lobe
- MeSH terms
- Adult, Aged, Aged, 80 and over, Alzheimer Disease, Brain, Cognition, Dementia, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Biomarkers, Amyloid beta-Peptides, Neurofibrillary Tangles, tau Proteins, Tauopathies, Positron-Emission Tomography, Presenilin-1, 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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