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PET Imaging of Neuroinflammation Using [11C]DPA-713 in a Mouse Model of Ischemic Stroke
Published on: June 14, 2018
Increased microglial activation in patients with Parkinson disease using [18F]-DPA714 TSPO PET imaging
Sonia Lavisse1, Sébastien Goutal1, Catriona Wimberley2
1Université Paris-Saclay, CEA, CNRS, MIRCen, Laboratoire des Maladies Neurodégénératives, 92265, Fontenay-aux-Roses, France.
Introduction:
Increasing evidence suggests that neuroinflammation is active in Parkinson disease (PD) and contributes to neurodegeneration. This process can be studied in vivo with PET and radioligands targeting TSPO, upregulated in activated microglia. Initial PET studies investigating microglial activation in PD with the [11C]-PK11195 have provided inconclusive results. Here we assess the presence and distribution of neuroinflammatory response in PD patients using [18F]-DPA714 and to correlate imaging biomarkers to dopamine transporter imaging and clinical status.
Methods:
PD patients (n = 24, Hoehn and Yahr I-III) and 28 healthy controls were scanned with [18F]-DPA714 and [11C]-PE2I and analyzed. They were all genotyped for TSPO polymorphism. Regional binding parameters were estimated (reference Logan graphical approach with supervised cluster analysis). Impact of TSPO genotype was analyzed using Wilcoxon signed-rank test. Differences between groups were investigated using a two-way ANOVA and Tukey post hoc tests.
Results:
PD patients showed significantly higher [18F]-DPA714 binding compared to healthy controls bilaterally in the midbrain (p < 0.001), the frontal cortex (p = 0.001), and the putamen contralateral to the more clinically affected hemibody (p = 0.038). Microglial activation in these regions did not correlate with the severity of motor symptoms, disease duration nor putaminal [11C]-PE2I uptake. However, there was a trend toward a correlation between cortical TSPO binding and disease duration (p = 0.015 uncorrected, p = 0.07 after Bonferroni correction).
Conclusion:
[18F]-DPA714 binding confirmed that there is a specific topographic pattern of microglial activation in the nigro-striatal pathway and the frontal cortex of PD patients.
Trial Registration:
Trial registration: INFLAPARK, NCT02319382. Registered 18 December 2014- Retrospectively registered, https://clinicaltrials.gov/ct2/show/NCT02319382.
Insights
This study shows increased microglial activation in Parkinson disease (PD) patients using [18F]-DPA714 PET imaging. Neuroinflammation was observed in the midbrain, frontal cortex, and putamen, but did not correlate with motor symptoms or disease duration.
Area of Science:
- Neuroscience
- Radiology
- Immunology
Background:
- Neuroinflammation, indicated by activated microglia, is increasingly recognized as a key factor in Parkinson disease (PD) pathogenesis and neurodegeneration.
- Positron Emission Tomography (PET) with radioligands targeting the translocator protein (TSPO), which is upregulated in activated microglia, offers a method for in vivo study of neuroinflammation.
- Previous PET studies using [11C]-PK11195 for microglial activation in PD yielded inconclusive results, necessitating further investigation with more advanced tracers.
Purpose of the Study:
- To assess the presence and topographical distribution of neuroinflammation in Parkinson disease (PD) patients using the TSPO-targeting PET tracer [18F]-DPA714.
- To investigate potential correlations between imaging biomarkers of microglial activation and dopamine transporter (DAT) imaging, as well as clinical status in PD patients.
- To evaluate the utility of [18F]-DPA714 as a reliable in vivo marker for neuroinflammation in Parkinson disease.
Main Methods:
- A cohort of 24 Parkinson disease (PD) patients (Hoehn and Yahr stages I-III) and 28 healthy controls underwent PET/CT scanning with [18F]-DPA714 and [11C]-PE2I.
- All participants were genotyped for the TSPO polymorphism, and its impact on tracer binding was analyzed.
- Regional binding parameters were estimated using the reference Logan graphical approach with supervised cluster analysis, and statistical comparisons were performed using two-way ANOVA and Tukey post hoc tests.
Main Results:
- PD patients exhibited significantly higher [18F]-DPA714 binding compared to healthy controls in the midbrain, frontal cortex, and the putamen contralateral to the more affected side.
- No significant correlation was found between microglial activation in these regions and motor symptom severity, disease duration, or putaminal [11C]-PE2I uptake.
- A trend toward correlation was observed between cortical TSPO binding and disease duration, although this did not reach statistical significance after Bonferroni correction.
Conclusions:
- [18F]-DPA714 PET imaging confirms a distinct topographic pattern of microglial activation within the nigro-striatal pathway and frontal cortex of Parkinson disease patients.
- The findings suggest that while neuroinflammation is present in specific brain regions in PD, its direct correlation with clinical parameters and DAT availability requires further investigation.
- This study highlights the potential of [18F]-DPA714 as a valuable tool for visualizing and quantifying neuroinflammation in Parkinson disease.
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