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PK11195 labels activated microglia in Alzheimer's disease and in vivo in a mouse model using PET
Open accessAbstract
Activated microglia may promote neurodegeneration in Alzheimer's disease (AD) and may also help in amyloid clearance in immunization therapies. In vivo imaging of activated microglia using positron emission tomography (PET) could assist in defining the role of activated microglia during AD progression and therapeutics. We hypothesized that PK11195, a ligand that binds activated microglia, could label these cells in postmortem AD tissues and in vivo in an animal model of AD using PET. [(3)H](R)-PK11195 binding was significantly higher in AD frontal cortex compared to controls and correlated mainly with the abundance of immunohistochemically labeled activated microglia. With age, the brains of APP/PS1 transgenic mice showed progressive increase in [(3)H](R)-PK11195 binding and [(11)C](R)-PK11195 retention in vivo assessed using microPET, which correlated with the histopathological abundance of activated microglia. These results suggest that PK11195 binding in AD postmortem tissue and transgenic mice in vivo correlates with the extent of microglial activation and may help define the role of activated microglia in the pathogenesis and treatment of AD.
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“It is generally accepted that microglia and macrophages are the primary cell types exhibiting an increased number of TSPO binding sites in human pathologies, and that astrocytes are not significant contributors to increased TSPO binding sites [44;45].”
From Expression of the translocator protein of 18 kDa by microglia, macrophages and astrocytes based on immunohistochemical localization in abnormal human brain (2009) · cites this paper as [44]
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Metadata
- Authors
- Venneti, S., Lopresti, B. J., Wang, G., Hamilton, R. L., Mathis, C. A., Klunk, W. E., Apte, U. M., & Wiley, C. A.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Wiley, Clayton A.
- ORCID
- Venue
- Neurobiology of Aging
- Publisher
- Elsevier BV
- Published
- 2009-08
- Volume
- 30
- Issue
- 8
- Pages
- 1217-1226
- ISSN
- 0197-4580 (ISSN-L)
- PMC
- PMC2745919
- OpenAlex
- W2011239875
- Cited by
- 138
- References
- 39
- Citations by year
- 2025: 3 · 2024: 6 · 2023: 3 · 2022: 8 · 2021: 9 · 2020: 11 · 2019: 9 · 2018: 9 · 2017: 11 · 2016: 8 · 2015: 10 · 2014: 13 · 2013: 7 · 2012: 13
- FWCI
- 3.96
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurobiology of Aging (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- University of Pittsburgh
- National Institutes of Health
- National Institute on Aging (R21AG025829, P50AG005133, R01AG020226, P50 AG05133-21)
- National Institute of Mental Health (R01 MH-64921, K24 MH01717, R01MH064921, K24MH001717, R01MH071151)
- 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
- PK11195, activated microglia, Alzheimer's disease, positron emission tomography, APP/PS1 mice, microglial activation, amyloid clearance, neurodegeneration, frontal cortex, radioligand binding, in vivo imaging
- MeSH terms
- Aged, Aged, 80 and over, Aging, Alzheimer Disease, Animals, Astrocytes, Brain, Disease Models, Animal, Female, Frontal Lobe, Humans, Isoquinolines, Male, Mice, Transgenic, Receptors, Cell Surface, Tritium, Amyloid beta-Protein Precursor, Microglia, Disease Progression, Positron-Emission Tomography, Mice, Presenilin-1, Protease Nexins
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