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Longitudinal assessment of Aβ and cognition in aging and Alzheimer disease
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OBJECTIVE: Assess Aβ deposition longitudinally and explore its relationship with cognition and disease progression. METHODS: Clinical follow-up was obtained 20 ± 3 months after [¹¹C]Pittsburgh compound B (PiB)-positron emission tomography in 206 subjects: 35 with dementia of the Alzheimer type (DAT), 65 with mild cognitive impairment (MCI), and 106 age-matched healthy controls (HCs). A second PiB scan was obtained at follow-up in 185 subjects and a third scan after 3 years in 57. RESULTS: At baseline, 97% of DAT, 69% of MCI, and 31% of HC subjects showed high PiB retention. At 20-month follow-up, small but significant increases in PiB standardized uptake value ratios were observed in the DAT and MCI groups, and in HCs with high PiB retention at baseline (5.7%, 2.1%, and 1.5%, respectively). Increases were associated with the number of apolipoprotein E ε4 alleles. There was a weak correlation between PiB increases and decline in cognition when all groups were combined. Progression to DAT occurred in 67% of MCI with high PiB versus 5% of those with low PiB, but 20% of the low PiB MCI subjects progressed to other dementias. Of the high PiB HCs, 16% developed MCI or DAT by 20 months and 25% by 3 years. One low PiB HC developed MCI. INTERPRETATION: Aβ deposition increases slowly from cognitive normality to moderate severity DAT. Extensive Aβ deposition precedes cognitive impairment, and is associated with ApoE genotype and a higher risk of cognitive decline in HCs and progression from MCI to DAT over 1 to 2 years. However, cognitive decline is only weakly related to change in Aβ burden, suggesting that downstream factors have a more direct effect on symptom progression.
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“and that progression of biomarker measures is also a continuous process that begins before symptoms [9–14]”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [13]
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“Numerous studies have shown that CU individuals with abnormal amyloid biomarkers have more rapid progression of atrophy, hypometabolism, and clinical/cognitive decline than individuals without biomarker evidence of Aβ deposition [13,33,80,93–99]”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [13]
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“The ε4 allele increased brain amyloid burden in a dose-dependent manner in normal elderly individuals and in mild cognitive impairment patients [93,94].”
From Plasma levels of apolipoprotein E, APOE genotype and risk of dementia and ischemic heart disease: A review (2016) · cites this paper as [94]
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“In a study characterizing sporadic AD, for instance, Villemagne et al. used Pittsburgh compound B (PiB) positron emission tomography (PET) to show that 31% of healthy control subjects had high PiB retention indicating Aß deposition and of these, 25% developed mild cognitive impairment or AD by 3 years (Villemagne et al., 2011).”
From Inhibiting USP16 rescues stem cell aging and memory in an Alzheimer’s model (2022) · cites this paper as Villemagne et al., 2011
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“Previous longitudinal studies have either failed to detect an early increase in regional Aβ deposition16 or identified a rather large early stage Aβ region including the posterior temporal, inferior parietal, posterior cingulate, precuneus, and occipital areas4.”
From Earliest accumulation of β-amyloid occurs within the default-mode network and concurrently affects brain connectivity (2017) · cites this paper as [16]
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Metadata
- Authors
- Villemagne, V. L., Pike, K. E., Chételat, G., Ellis, K. A., Mulligan, R. S., Bourgeat, P., Ackermann, U., Jones, G., Szoeke, C., Salvado, O., Martins, R., O'Keefe, G., Mathis, C. A., Klunk, W. E., Ames, D., Masters, C. L., & Rowe, C. C.
- Affiliations
- Mental Health Research Institute (AU)
- Austin Health (AU)
- Commonwealth Scientific and Industrial Research Organisation (AU)
- Australian e-Health Research Centre (AU)
- Edith Cowan University (AU)
- University of Pittsburgh (US)
- National Ageing Research Institute (AU)
- The University of Melbourne (AU)
- Corresponding author
- Villemagne, Victor L.
- ORCID
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2011-01
- Volume
- 69
- Issue
- 1
- Pages
- 181-192
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- PMC
- PMC3045039
- OpenAlex
- W2051489981
- Cited by
- 833
- References
- 42
- Citations by year
- 2026: 28 · 2025: 32 · 2024: 26 · 2023: 51 · 2022: 42 · 2021: 44 · 2020: 57 · 2019: 60 · 2018: 57 · 2017: 57 · 2016: 60 · 2015: 61 · 2014: 68 · 2013: 86 · 2012: 71
- FWCI
- 57.02
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- UWA Profiles and Research Repository (UWA) (submittedVersion)
- Edith Cowan University Research Online (Edith Cowan University) (submittedVersion)
- Funders
- National Institute on Aging (P01AG025204, RF1AG025516, P50AG005133, R37AG025516)
- 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 › Oncology › Cancer-related cognitive impairment studies
- Keywords
- amyloid-beta deposition, Alzheimer's disease, mild cognitive impairment, Pittsburgh compound B PET, APOE ε4, cognitive decline, disease progression, aging
- MeSH terms
- Aged, Aging, Alzheimer Disease, Aniline Compounds, Brain, Cognition, Cognition Disorders, Female, Follow-Up Studies, Humans, Longitudinal Studies, Magnetic Resonance Imaging, Male, Neuropsychological Tests, Polymorphism, Genetic, Severity of Illness Index, Thiazoles, Amyloid beta-Peptides, Disease Progression, Positron-Emission Tomography, Plaque, Amyloid
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