A multicentre longitudinal study of flortaucipir (18F) in normal ageing, mild cognitive impairment and Alzheimer’s disease dementia
Open accessAbstract
The advent of tau-targeted PET tracers such as flortaucipir (18F) (flortaucipir, also known as 18F-AV-1451 or 18F-T807) have made it possible to investigate the sequence of development of tau in relationship to age, amyloid-β, and to the development of cognitive impairment due to Alzheimer's disease. Here we report a multicentre longitudinal evaluation of the relationships between baseline tau, tau change and cognitive change, using flortaucipir PET imaging. A total of 202 participants 50 years old or older, including 57 cognitively normal subjects, 97 clinically defined mild cognitive impairment and 48 possible or probable Alzheimer's disease dementia patients, received flortaucipir PET scans of 20 min in duration beginning 80 min after intravenous administration of 370 MBq flortaucipir (18F). On separate days, subjects also received florbetapir amyloid PET imaging, and underwent a neuropsychological test battery. Follow-up flortaucipir scans and neuropsychological battery assessments were also performed at 9 and 18 months. Fifty-five amyloid-β+ and 90 amyloid-β- subjects completed the baseline and 18-month study visits and had valid quantifiable flortaucipir scans at both time points. There was a statistically significant increase in the global estimate of cortical tau burden as measured by standardized uptake value ratio (SUVr) from baseline to 18 months in amyloid-β+ but not amyloid-β- subjects (least squared mean change in flortaucipir SUVr : 0.0524 ± 0.0085, P < 0.0001 and 0.0007 ± 0.0024 P = 0.7850, respectively), and a significant association between magnitude of SUVr increase and baseline tau burden. Voxel-wise evaluations further suggested that the regional pattern of change in flortaucipir PET SUVr over the 18-month study period (i.e. which regions exhibited the greatest change) also varied as a function of baseline global estimate of tau burden. In subjects with lower global SUVr, temporal lobe regions showed the greatest flortaucipir retention, whereas in subjects with higher baseline SUVr, parietal and frontal regions were increasingly affected. Finally, baseline flortaucipir and change in flortaucipir SUVr were both significantly (P < 0.0001) associated with changes in cognitive performance. Taken together, these results provide a preliminary characterization of the longitudinal spread of tau in Alzheimer's disease and suggest that the amount and location of tau may have implications both for the spread of tau and the cognitive deterioration that may occur over an 18-month period.
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Aβ deposition is a necessary antecedent for spread of tau beyond the temporal lobe in AD.
“Longitudinal deposition in tau PET is associated with baseline levels tau and Aβ deposition is a necessary antecedent for spread of tau beyond the temporal lobe in AD [189, 190] (Fig. 3).”
From The use of neuroimaging techniques in the early and differential diagnosis of dementia (2023) · cites this paper as [190]
The Discussion (page unavailable) reports no measurable tau-PET change in the amyloid-β− group over 18 months, compared with significant change in the amyloid-β+ group. It says this suggests amyloid deposition *may* be a necessary antecedent for spread beyond the temporal lobe in Alzheimer’s disease; the claim presents that tentative inference as established fact. (LLM, conf=0.91)
Experimental — accuracy not yet measuredLongitudinal deposition in tau PET is associated with baseline levels of tau.
“Longitudinal deposition in tau PET is associated with baseline levels tau and Aβ deposition is a necessary antecedent for spread of tau beyond the temporal lobe in AD [189, 190] (Fig. 3).”
From The use of neuroimaging techniques in the early and differential diagnosis of dementia (2023) · cites this paper as [190]
The pattern of tau pathology can differ substantially between individuals.
“the pattern of tau pathology can differ significantly from person to person”
From The amyloid hypothesis in Alzheimer disease: new insights from new therapeutics (2022) · cites this paper as [25]
Aβ deposition may be required for progression of tau pathology in AD.
“Several lines of evidence suggest Aβ deposition may be required for progression of tau pathology in AD”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Pontecorvo et al., 2019
In human neuropathological studies, tau pathology generally does not progress from the entorhinal cortex into the neocortex without co-occurring amyloid pathology.
“Neuropathological studies in humanshave demonstrated that tau pathology generally does not progress from the entorhinal cortex into the neocortex in the absence of co-occurring amyloid pathology”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Pontecorvo et al., 2019
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Self-citation
- Authors
- Pontecorvo, M. J., Devous, M. D., Kennedy, I., Navitsky, M., Lu, M., Galante, N., Salloway, S., Doraiswamy, P. M., Southekal, S., Arora, A. K., McGeehan, A., Lim, N. C., Xiong, H., Truocchio, S. P., Joshi, A. D., Shcherbinin, S., Teske, B., Fleisher, A. S., & Mintun, M. A.
- Affiliations
- Avid Radiopharmaceuticals (United States) (US)
- Butler Hospital (US)
- Duke University Health System (US)
- Eli Lilly (United States) (US)
- Corresponding author
- Pontecorvo, Michael J
- Joshi, Abhinay D
- ORCID
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2019-04-22
- Volume
- 142
- Issue
- 6
- Pages
- 1723-1735
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC6536847
- OpenAlex
- W2942151633
- Cited by
- 249
- References
- 70
- Citations by year
- 2026: 14 · 2025: 31 · 2024: 41 · 2023: 41 · 2022: 36 · 2021: 42 · 2020: 32 · 2019: 11
- FWCI
- 24.05
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Brain (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- Avid Radiopharmaceuticals
- Eli Lilly and Company
- Functional Neuromodulation
- 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
- tau PET imaging, tau burden, Alzheimer's disease, mild cognitive impairment, normal aging, amyloid-beta, florbetapir, standardized uptake value ratio, cognitive decline, temporal lobe, amyloid PET, neurodegeneration
- MeSH terms
- Aged, Aging, Alzheimer Disease, Amyloid, Brain, Carbolines, Cognition, Cognition Disorders, Dementia, Female, Humans, Longitudinal Studies, Male, Middle Aged, Amyloid beta-Peptides, tau Proteins, Cognitive Dysfunction
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