The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
In vivo changes in microglial activation and amyloid deposits in brain regions with hypometabolism in Alzheimer’s disease
Open accessAbstract
Purpose Amyloid β protein (Aβ) is known as a pathological substance in Alzheimer's disease (AD) and is assumed to coexist with a degree of activated microglia in the brain. However, it remains unclear whether these two events occur in parallel with characteristic hypometabolism in AD in vivo. The purpose of the present study was to clarify the in vivo relationship between Aβ accumulation and neuroinflammation in those specific brain regions in early AD.Methods Eleven nootropic drug-naïve AD patients underwent a series of positron emission tomography (PET) measurements with [(11)C](R)PK11195, [(11)C]PIB and [(18)F]FDG and a battery of cognitive tests within the same day. The binding potentials (BPs) of [(11)C](R)PK11195 were directly compared with those of [(11)C]PIB in the brain regions with reduced glucose metabolism.Results BPs of [(11)C](R)PK11195 and [(11)C]PIB were significantly higher in the parietotemporal regions of AD patients than in ten healthy controls. In AD patients, there was a negative correlation between dementia score and [(11)C](R)PK11195 BPs, but not [(11)C]PIB, in the limbic, precuneus and prefrontal regions. Direct comparisons showed a significant negative correlation between [(11)C](R)PK11195 and [(11)C]PIB BPs in the posterior cingulate cortex (PCC) (p < 0.05, corrected) that manifested the most severe reduction in [(18)F]FDG uptake.Conclusion A lack of coupling between microglial activation and amyloid deposits may indicate that Aβ accumulation shown by [(11)C]PIB is not always the primary cause of microglial activation, but rather the negative correlation present in the PCC suggests that microglia can show higher activation during the production of Aβ in early AD.
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“AD patients all showed significantly increased regional TSPO ligand binding in the cortices compared to controls.”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [136]
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Metadata
- Authors
- Yokokura, M., Mori, N., Yagi, S., Yoshikawa, E., Kikuchi, M., Yoshihara, Y., Wakuda, T., Sugihara, G., Takebayashi, K., Suda, S., Iwata, Y., Ueki, T., Tsuchiya, K. J., Suzuki, K., Nakamura, K., & Ouchi, Y.
- Affiliations
- Hamamatsu University School of Medicine (JP)
- Hamamatsu University (JP)
- Hamamatsu Photonics (Japan) (JP)
- Kanazawa University (JP)
- Corresponding author
- Ouchi, Yasuomi
- ORCID
- Venue
- European Journal of Nuclear Medicine and Molecular Imaging
- Published
- 2010-09-16
- Volume
- 38
- Issue
- 2
- Pages
- 343-351
- ISSN
- 1619-7070 (ISSN-L)
- 1619-7089
- OpenAlex
- W1991282216
- Cited by
- 174
- References
- 42
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 6 · 2023: 9 · 2022: 13 · 2021: 12 · 2020: 13 · 2019: 18 · 2018: 11 · 2017: 17 · 2016: 14 · 2015: 14 · 2014: 10 · 2013: 9 · 2012: 10
- FWCI
- 5.63
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- cc-by-nc-nd
- www.springer.com/tdm (tdm)
- Locations
- European Journal of Nuclear Medicine and Molecular Imaging (publishedVersion)
- PubMed (publishedVersion)
- HamaMed-Repository (Hamamatsu University School of Medicine) (submittedVersion, cc-by-nc-nd)
- Funders
- Japan Society for the Promotion of Science (22591260, 23390287, 22591258, 23659562)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, microglial activation, amyloid-beta, hypometabolism, neuroinflammation, PK11195, Pib, FDG-PET, posterior cingulate cortex, early Alzheimer's disease
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Brain, Female, Glucose, Humans, Male, Middle Aged, Neurons, Radioactive Tracers, Case-Control Studies, Amyloid beta-Peptides, Microglia, Positron-Emission Tomography
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