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Amyloid PET imaging in patients with mild cognitive impairment: A 2-year follow-up study
Abstract
BACKGROUND: Patients with amnestic mild cognitive impairment (MCI) have greater risk of conversion to Alzheimer disease (AD). Increased brain amyloid burden in AD and MCI has been demonstrated with PET using [(11)C] Pittsburgh compound B (PiB) as a tracer. OBJECTIVE: To evaluate change in β-amyloid deposition in with MCI during 2-year follow-up. METHODS: Patients with MCI and controls were studied with [(11)C] PiB PET, MRI, and neuropsychometry at baseline and these investigations were repeated in patients with MCI after follow-up. RESULTS: Those patients with MCI converting to AD during follow-up had greater [(11)C] PiB retention in the posterior cingulate (p=0.020), in the lateral frontal cortex (p=0.006), in the temporal cortex (p=0.022), in the putamen (p=0.041), and in the caudate nucleus (p=0.025) as compared to nonconverters. In converters, there was no significant change in [(11)C] PiB uptake, whereas an increase was seen as compared to baseline in nonconverters in the anterior and posterior cingulate, temporal and parietal cortices, and putamen. Hippocampal atrophy was greater in converters at baseline than in nonconverters, but increased significantly in both groups during follow-up. CONCLUSIONS: Hippocampal atrophy and amyloid deposition seem to dissociate during the evolution of MCI, the atrophy increasing clearly and [(11)C] PiB retention changing modestly when conversion to AD occurs. Longer follow-up is needed to determine whether nonconverters would convert to AD later, which would suggest accelerated [(11)C] PiB retention preceding clinical conversion.
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“indicating a fundamental participation of microglia in the development and progression of AD.”
From Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation (2019) · cites this paper as [151]
In the citing paper
“PET imaging studies have shown that subjects with high amounts of amyloid-β, but no dementia, had decreased microglia activation [151–153]”
From Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation (2019) · cites this paper as [151]
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Metadata
- Authors
- Koivunen, J., Scheinin, N., Virta, J. R., Aalto, S., Vahlberg, T., Någren, K., Helin, S., Parkkola, R., Viitanen, M., & Rinne, J. O.
- Affiliations
- University of Turku (FI)
- ORCID
- Venue
- Neurology
- Published
- 2011-03-22
- Volume
- 76
- Issue
- 12
- Pages
- 1085-1090
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W2143282099
- Cited by
- 188
- References
- 18
- Citations by year
- 2026: 6 · 2025: 1 · 2024: 4 · 2023: 6 · 2022: 6 · 2021: 11 · 2020: 5 · 2019: 12 · 2018: 9 · 2017: 8 · 2016: 12 · 2015: 12 · 2014: 27 · 2013: 30 · 2012: 32
- FWCI
- 21.01
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurology (publishedVersion)
- PubMed (publishedVersion)
- 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
- amnestic mild cognitive impairment, amyloid-beta deposition, Pittsburgh compound B, amyloid PET, hippocampal atrophy, posterior cingulate cortex, temporal cortex, putamen, longitudinal follow-up
- MeSH terms
- Aged, Alzheimer Disease, Aniline Compounds, Atrophy, Brain, Carbon Radioisotopes, Cognition Disorders, Female, Follow-Up Studies, Humans, Male, Neuropsychological Tests, Thiazoles, Amyloid beta-Peptides, Disease Progression, Positron-Emission Tomography
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