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Cited by 180Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsMedical Imaging Techniques and Applications

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Distinct 18F-AV-1451 tau PET retention patterns in early- and late-onset Alzheimer’s disease

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Schöll, Michael, Ossenkoppele, Rik, Strandberg, Olof, Palmqvist, Sebastian, The Swedish BioFINDER study, Jögi, Jonas, Ohlsson, Tomas, Smith, Ruben, Hansson, Oskar·2017·Brain
DOI 10.1093/brain/awx171
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Abstract

Patients with Alzheimer's disease can present with different clinical phenotypes. Individuals with late-onset Alzheimer's disease (>65 years) typically present with medial temporal lobe neurodegeneration and predominantly amnestic symptomatology, while patients with early-onset Alzheimer's disease (<65 years) exhibit greater neocortical involvement associated with a clinical presentation including dyspraxia, executive dysfunction, or visuospatial impairment. We recruited 20 patients with early-onset Alzheimer's disease, 21 with late-onset Alzheimer's disease, three with prodromal early-onset Alzheimer's disease and 13 with prodromal late-onset Alzheimer's disease, as well as 30 cognitively healthy elderly controls, that had undergone 18F-AV-1451 tau positron emission tomography and structural magnetic resonance imaging to explore whether early- and late-onset Alzheimer's disease exhibit differential regional tau pathology and atrophy patterns. Strong associations of lower age at symptom onset with higher 18F-AV-1451 uptake were observed in several neocortical regions, while higher age did not yield positive associations in neither patient group. Comparing patients with early-onset Alzheimer's disease with controls resulted in significantly higher 18F-AV-1451 retention throughout the neocortex, while comparing healthy controls with late-onset Alzheimer's disease patients yielded a distinct pattern of higher 18F-AV-1451 retention, predominantly confined to temporal lobe regions. When compared against each other, the early-onset Alzheimer's disease group exhibited greater uptake than the late-onset group in prefrontal and premotor, as well as in inferior parietal cortex. These preliminary findings indicate that age may constitute an important contributor to Alzheimer's disease heterogeneity highlighting the potential of tau positron emission tomography to capture phenotypic variation across patients with Alzheimer's disease.

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Crossref · 10.1093/brain/awx171

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Figures

Figure 1 Group differences in 18 F-AV-1451 and cortical atrophy. T-maps showing the results of voxelwise ANCOVA and two-sample t -test analyses. ( A ) Showing higher 18 F-AV-1451 uptake in early-onset Alzheimer's disease (EOAD) subjects when compared to healthy controls (HC), higher AV-1451 uptake in late-onset Alzheimer's disease (LOAD) subjects when compared to healthy controls (ANCOVA; both P 5 0.05, FWE), and higher 18 F-AV-1451 uptake in patients with early-onset Alzheimer's disease when compared to late-onset Alzheimer's disease patients ( t -test) ( P 5 0.001, uncorrected). ( B ) Greater grey matter atrophy in early-onset Alzheimer's disease and late-onset Alzheimer's disease patients when compared with healthy controls (ANCOVA; P 5 0.001 uncorrected). No voxels survived statistically at this threshold when comparing early-onset Alzheimer's disease directly to late-onset Alzheimer's disease. VBM = voxel-based morphometry.
Figure 1 Group differences in 18 F-AV-1451 and cortical atrophy. T-maps showing the results of voxelwise ANCOVA and two-sample t -test analyses. ( A ) Showing higher 18 F-AV-1451 uptake in early-onset Alzheimer's disease (EOAD) subjects when compared to healthy controls (HC), higher AV-1451 uptake in late-onset Alzheimer's disease (LOAD) subjects when compared to healthy controls (ANCOVA; both P 5 0.05, FWE), and higher 18 F-AV-1451 uptake in patients with early-onset Alzheimer's disease when compared to late-onset Alzheimer's disease patients ( t -test) ( P 5 0.001, uncorrected). ( B ) Greater grey matter atrophy in early-onset Alzheimer's disease and late-onset Alzheimer's disease patients when compared with healthy controls (ANCOVA; P 5 0.001 uncorrected). No voxels survived statistically at this threshold when comparing early-onset Alzheimer's disease directly to late-onset Alzheimer's disease. VBM = voxel-based morphometry.CC-BY-NC · From the PDF
Figure 2 18 F-AV-1451 uptake in Braak regions of interest and effect of continuous age on 18 F-AV-1451 uptake. ( A ) Box plots displaying 18 F-AV-1451 uptake in regions of interest approximating Braak stages of tau pathology. All patient groups had higher uptake than the controls in each region of interest (all P 5 0.001). ( B-D ) Scatter plots displaying the relationship between age at symptom onset (for established and prodromal Alzheimer's disease patients, age at PETexamination for healthy controls) and 18 F-AV-1451 uptake in Braak regions of interest. ( EG ) Voxelwise multiple regressions of continous age (at symptom onset for patients, at PET examination for healthy controls) on 18 F-AV-1451 uptake. Higher age showed a tendency to be associated with higher 18 F-AV-1451 uptake predominantly in medial temporal lobe ( P 5 0.01, uncorrected) ( E ), while lower age was associated with higher ligand uptake in regions corresponding to Braak regions of interest III/IV (prodromal Alzheimer's disease, pAD) ( F ) and Braak III-VI (Alzheimer's disease, AD) ( G ). EOAD = early-onset Alzheimer's disease; EOpAD = early-onset prodromal Alzheimer's disease; LOAD = late-onset Alzheimer's disease; LOpAD = late-onset prodromal Alzheimer's disease; HC = healthy controls; ROI = region of interest.
Figure 2 18 F-AV-1451 uptake in Braak regions of interest and effect of continuous age on 18 F-AV-1451 uptake. ( A ) Box plots displaying 18 F-AV-1451 uptake in regions of interest approximating Braak stages of tau pathology. All patient groups had higher uptake than the controls in each region of interest (all P 5 0.001). ( B-D ) Scatter plots displaying the relationship between age at symptom onset (for established and prodromal Alzheimer's disease patients, age at PETexamination for healthy controls) and 18 F-AV-1451 uptake in Braak regions of interest. ( EG ) Voxelwise multiple regressions of continous age (at symptom onset for patients, at PET examination for healthy controls) on 18 F-AV-1451 uptake. Higher age showed a tendency to be associated with higher 18 F-AV-1451 uptake predominantly in medial temporal lobe ( P 5 0.01, uncorrected) ( E ), while lower age was associated with higher ligand uptake in regions corresponding to Braak regions of interest III/IV (prodromal Alzheimer's disease, pAD) ( F ) and Braak III-VI (Alzheimer's disease, AD) ( G ). EOAD = early-onset Alzheimer's disease; EOpAD = early-onset prodromal Alzheimer's disease; LOAD = late-onset Alzheimer's disease; LOpAD = late-onset prodromal Alzheimer's disease; HC = healthy controls; ROI = region of interest.CC-BY-NC · From the PDF
Figure 3 18 F-AV-1451 retention patterns in autosomal-dominant and sporadic Alzheimer's disease. ( A ) Surface renderings of the 18 F-AV-1451 scans of two symptomatic PSEN1 mutation carriers in contrast to the averaged 18 F-AV-1451 scans of all early-onset Alzheimer's disease (EOAD, B ) and late-onset Alzheimer's disease subjects (LOAD, C ). AD = Alzheimer's disease; MCI = mild cognitive impairment; MMSE = Mini-Mental State Examination; SUVR = standardized uptake value ratio.
Figure 3 18 F-AV-1451 retention patterns in autosomal-dominant and sporadic Alzheimer's disease. ( A ) Surface renderings of the 18 F-AV-1451 scans of two symptomatic PSEN1 mutation carriers in contrast to the averaged 18 F-AV-1451 scans of all early-onset Alzheimer's disease (EOAD, B ) and late-onset Alzheimer's disease subjects (LOAD, C ). AD = Alzheimer's disease; MCI = mild cognitive impairment; MMSE = Mini-Mental State Examination; SUVR = standardized uptake value ratio.CC-BY-NC · From the PDF

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Metadata

Authors
Schöll, M., Ossenkoppele, R., Strandberg, O., Palmqvist, S., study, T. S. B., Jögi, J., Ohlsson, T., Smith, R., & Hansson, O.
Affiliations
  • Lund University (SE)
  • Amsterdam Neuroscience (NL)
  • Skåne University Hospital (SE)
Corresponding author
Schöll, Michael
ORCID
Venue
Brain
Publisher
Oxford University Press (OUP)
Published
2017-07-16
Volume
140
Issue
9
Pages
2286-2294
ISSN
  • 0006-8950 (ISSN-L)
  • 1460-2156
DOI
10.1093/brain/awx171
OpenAlex
W2751819353
Cited by
180
References
28
Citations by year
2026: 8 · 2025: 19 · 2024: 13 · 2023: 24 · 2022: 17 · 2021: 30 · 2020: 29 · 2019: 23 · 2018: 16 · 2017: 1
FWCI
15.50
Type
journal article
Language
en
Open access
Licence
Locations
  • Brain (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • Pure Amsterdam UMC (publishedVersion, other-oa)
  • Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
  • UCL Discovery (University College London) (submittedVersion)
  • Lund University Publications (Lund University) (submittedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion)
Funders
  • European Research Council
  • Swedish Research Council
  • Swedish Brain Foundation
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Medical Imaging Techniques and Applications
Keywords
Alzheimer's disease, early-onset Alzheimer's disease, late-onset Alzheimer's disease, 18F-AV-1451, tau PET, age at symptom onset, prodromal Alzheimer's disease, temporal lobe atrophy, prefrontal cortex, inferior parietal cortex, disease heterogeneity, clinical phenotype
MeSH terms
Aged, Aging, Alzheimer Disease, Atrophy, Carbolines, Cerebral Cortex, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Case-Control Studies, tau Proteins, Age of Onset, Tauopathies, Positron-Emission Tomography, Neuroimaging, Prodromal Symptoms

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