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Imaging microglial activation and glucose consumption in a mouse model of Alzheimer's disease
Sara Rapic1, Heiko Backes, Thomas Viel
1European Institute for Molecular Imaging, Westfalian Wilhelms-University Münster, Münster, Germany.
Abstract:
In Alzheimer's disease (AD), persistent microglial activation as sign of chronic neuroinflammation contributes to disease progression. Our study aimed to in vivo visualize and quantify microglial activation in 13- to 15-month-old AD mice using [(11)C]-(R)-PK11195 and positron emission tomography (PET). We attempted to modulate neuroinflammation by subjecting the animals to an anti-inflammatory treatment with pioglitazone (5-weeks' treatment, 5-week wash-out period). [(11)C]-(R)-PK11195 distribution volume values in AD mice were significantly higher compared with control mice after the wash-out period at 15 months, which was supported by immunohistochemistry data. However, [(11)C]-(R)-PK11195 μPET could not demonstrate genotype- or treatment-dependent differences in the 13- to 14-month-old animals, suggesting that microglial activation in AD mice at this age and disease stage is too mild to be detected by this imaging method.
Insights
In Alzheimer's disease (AD), microglial activation is a key indicator of neuroinflammation. This study used PET imaging to visualize microglial activation in AD mice, finding increased activation in older mice but not detecting it in younger ones.
Area of Science:
- Neuroscience
- Immunology
- Radiochemistry
Background:
- Persistent microglial activation signifies chronic neuroinflammation in Alzheimer's disease (AD), driving disease progression.
- Neuroinflammation, characterized by microglial activation, is a critical factor in Alzheimer's disease pathogenesis.
Purpose of the Study:
- To visualize and quantify in vivo microglial activation in 13- to 15-month-old AD mice using [(11)C]-(R)-PK11195 and positron emission tomography (PET).
- To assess the potential of pioglitazone treatment to modulate neuroinflammation in AD mice.
Main Methods:
- Utilized [(11)C]-(R)-PK11195 and microPET imaging to assess microglial activation in AD mice.
- Administered pioglitazone as an anti-inflammatory treatment, followed by a 5-week wash-out period.
- Correlated PET findings with immunohistochemistry data.
Main Results:
- [(11)C]-(R)-PK11195 distribution volume values were significantly higher in 15-month-old AD mice compared to controls post-washout, confirmed by immunohistochemistry.
- MicroPET imaging did not reveal genotype- or treatment-dependent differences in 13- to 14-month-old animals.
- The study suggests that microglial activation in younger AD mice (13-14 months) is too subtle for detection by current [(11)C]-(R)-PK11195 PET imaging.
Conclusions:
- [(11)C]-(R)-PK11195 PET imaging can detect increased microglial activation in aged AD mice.
- The sensitivity of [(11)C]-(R)-PK11195 PET for detecting neuroinflammation in early-stage AD mouse models may be limited.
- Further research is needed to optimize imaging techniques for early detection of neuroinflammation in Alzheimer's disease.
