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Microglia, amyloid, and cognition in Alzheimer's disease: An [11C](R)PK11195-PET and [11C]PIB-PET study
Open accessAbstract
[11C](R)PK11195-PET is a marker of activated microglia while [11C]PIB-PET detects raised amyloid load. Here we studied in vivo the distributions of amyloid load and microglial activation in Alzheimer's disease (AD) and their relationship with cognitive status. Thirteen AD subjects had [11C](R)PK11195-PET and [11C]PIB-PET scans. Ten healthy controls had [11C](R)PK11195-PET and 14 controls had [11C]PIB-PET scans. Region-of-interest analysis of [11C](R)PK11195-PET detected significant 20-35% increases in microglial activation in frontal, temporal, parietal, occipital and cingulate cortices (p<0.05) of the AD subjects. [11C]PIB-PET revealed significant two-fold increases in amyloid load in these same cortical areas (p<0.0001) and SPM (statistical parametric mapping) analysis confirmed the localisation of these increases to association areas. MMSE scores in AD subjects correlated with levels of cortical microglial activation but not with amyloid load. The inverse correlation between MMSE and microglial activation is compatible with a role of microglia in neuronal damage.
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“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 [153]
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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 [153]
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Metadata
- Authors
- Edison, P., Archer, H. A., Gerhard, A., Hinz, R., Pavese, N., Turkheimer, F. E., Hammers, A., Tai, Y. F., Fox, N., Kennedy, A., Rossor, M., & Brooks, D. J.
- Affiliations
- Hammersmith Hospital (GB)
- University of Manchester (GB)
- Corresponding author
- Edison, Paul
- ORCID
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2008-12
- Volume
- 32
- Issue
- 3
- Pages
- 412-419
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W1993305977
- Cited by
- 513
- References
- 55
- Citations by year
- 2026: 9 · 2025: 19 · 2024: 21 · 2023: 16 · 2022: 27 · 2021: 40 · 2020: 29 · 2019: 32 · 2018: 27 · 2017: 44 · 2016: 39 · 2015: 40 · 2014: 46 · 2013: 33 · 2012: 31
- FWCI
- 12.97
- Type
- journal article
- Language
- en
- Open access
- green
- doaj.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- UCL Discovery (University College London) (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- Research Explorer (The University of Manchester) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- Medical Research Council
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, microglial activation, amyloid-beta, cognitive impairment, [11C](R)-PK11195, [11C]PIB, positron emission tomography, association cortex, Mini-Mental State Examination, neuroinflammation, neuronal injury
- MeSH terms
- Aged, Alzheimer Disease, Amyloid, Aniline Compounds, Carbon Radioisotopes, Cerebral Cortex, Cognition, Female, Humans, Isoquinolines, Magnetic Resonance Imaging, Male, Middle Aged, Thiazoles, Cluster Analysis, Microglia, Positron-Emission Tomography
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