Microglial activation and amyloid deposition in mild cognitive impairment: A PET study
Open accessAbstract
BACKGROUND: Activated microglia may play a role in the pathogenesis of Alzheimer disease (AD) as they cluster around beta-amyloid (Abeta) plaques. They are, therefore, a potential therapeutic target in both AD and its prodrome amnestic mild cognitive impairment (MCI). OBJECTIVE: To characterize in vivo with (11)C-(R)-PK11195 and (11)C-PIB PET the distribution of microglial activation and amyloid deposition in patients with amnestic MCI. METHODS: Fourteen subjects with MCI had (11)C-(R)-PK11195 and (11)C-PIB PET with psychometric tests. RESULTS: Seven out of 14 (50%) patients with MCI had increased cortical (11)C-PIB retention (p < 0.001) while 5 out of 13 (38%) subjects with MCI showed increased (11)C-(R)-PK11195 uptake. The MCI subgroup with increased (11)C-PIB retention also showed increased cortical (11)C-(R)-PK11195 binding (p < 0.036) though this increase only remained significant in frontal cortex after a correction for multiple comparisons. There was no correlation between regional levels of (11)C-(R)-PK11195 and (11)C-PIB binding in individual patients with MCI: only three of the five MCI cases with increased (11)C-(R)-PK11195 binding had increased levels of (11)C-PIB retention. CONCLUSIONS: Our findings indicate that, while amyloid deposition and microglial activation can be detected in vivo in around 50% of patients with mild cognitive impairment (MCI), these pathologies can occur independently. The detection of microglial activation in patients with MCI suggests that anti-inflammatory therapies may be relevant to the prevention of AD.
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With other pathologies e.g. in Alzheimer's disease, the interpretation of increased TSPO PET signal also may reflect differences in relative abundance of microglia and astrocytes.
“With other pathologies e.g. in Alzheimer’s disease (Okello et al., 2009), the interpretation of increased TSPO PET signal also may reflect differences in relative abundance of microglia and astrocytes.”
From A quantitative neuropathological assessment of translocator protein expression in multiple sclerosis (2019) · cites this paper as Okello et al., 2009
The Results and discussion (indexed as GLOSSARY; page unavailable) report increased PK11195 binding in an MCI subgroup and discuss increased binding in Alzheimer’s disease. They do not address astrocytes or suggest that the PET signal reflects the relative abundance of microglia and astrocytes. (LLM, conf=0.84)
Experimental — accuracy not yet measuredMicroglial activation is detected by PET in patients with mild cognitive impairment (MCI).
“Microglial activation has also been detected by PET in patients with mild cognitive impairment (MCI).”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [140]
Microglia fundamentally participate in the development and progression of Alzheimer's disease.
“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 [152]
In subjects with high amounts of amyloid-β but no dementia, PET imaging shows decreased microglia activation.
“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 [152]
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References 41 · Cited by 367
Research works printed but not linked: 1
- [31]31. Mintun MA, Larossa GN, Sheline YI, et al. [11C]PIB in a nondemented population: potential antecedent marker of Alzheimer disease. Neurology 2006;67:446-452.
- Authors
- Okello, A., Edison, P., Archer, H. A., Turkheimer, F. E., Kennedy, J., Bullock, R., Walker, Z., Kennedy, A., Fox, N., Rossor, M., & Brooks, D. J.
- Affiliations
- UCL Queen Square Institute of Neurology (GB)
- Venue
- Neurology
- Published
- 2009-01-06
- Volume
- 72
- Issue
- 1
- Pages
- 56-62
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- PMC
- PMC2817573
- OpenAlex
- W2044488773
- Cited by
- 367
- References
- 41
- Citations by year
- 2026: 7 · 2025: 11 · 2024: 18 · 2023: 19 · 2022: 15 · 2021: 30 · 2020: 18 · 2019: 25 · 2018: 16 · 2017: 20 · 2016: 25 · 2015: 18 · 2014: 31 · 2013: 30 · 2012: 28
- FWCI
- 17.32
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Neurology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Research Portal (King's College London) (submittedVersion)
- Pure Amsterdam UMC (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- microglial activation, amyloid deposition, amnestic mild cognitive impairment, Alzheimer's disease, positron emission tomography, amyloid plaques, anti-inflammatory therapy, frontal cortex
- MeSH terms
- Aged, Alzheimer Disease, Aniline Compounds, Brain Mapping, Carbon Radioisotopes, Cognition Disorders, Female, Follow-Up Studies, Humans, Isoquinolines, Magnetic Resonance Imaging, Male, Middle Aged, Neuropsychological Tests, Thiazoles, Amyloid beta-Peptides, Microglia, Positron-Emission Tomography, Benzothiazoles
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