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PET Imaging of Neuroinflammation Using [11C]DPA-713 in a Mouse Model of Ischemic Stroke
Published on: June 14, 2018
Time course of neuroinflammation after human stroke - a pilot study using co-registered PET and MRI
Lucio D'Anna1,2, Graham Searle3, Kirsten Harvey2
1Department of Stroke and Neuroscience, Charing Cross Hospital, Imperial College Healthcare NHS Trust, London, UK.
Background:
Microglial activation contributes to both inflammatory damage and repair in experimental ischemic stroke. However, because of the logistical challenges, there have been few clinical imaging studies directly describing inflammatory activation and its resolution after stroke. The purpose of our pilot study was to describe the spatio-temporal profile of brain inflammation after stroke using 18kD translocator protein (TSPO) positron emission tomography (PET) with magnetic resonance (MR) co-registration in the subacute and chronic stage after stroke.
Methods:
Three patients underwent magnetic resonance imaging (MRI) and PET scans with TSPO ligand [11C]PBR28 15 ± 3 and 90 ± 7 days after an ischaemic stroke. Regions of interest (ROI) were defined on MRI images and applied to the dynamic PET data to derive regional time-activity curves. Regional uptake was quantified as standardised uptake values (SUV) over 60 to 90 min post-injection. ROI analysis was applied to identify binding in the infarct, and in frontal, temporal, parietal, and occipital lobes and cerebellum excluding the infarcted area.
Results:
The mean age of participants was 56 ± 20.4 years and mean infarct volume was 17.9 ± 18.1 ml. [11C]PBR28 showed increased tracer signal in the infarcted area compared to non-infarcted areas of the brain in the subacute phase of stroke (Patient 1 SUV 1.81; Patient 2 SUV 1.15; Patient 3 SUV 1.64). [11C]PBR28 uptake returned to the level of non-infarcted areas at 90 days Patient 1 SUV 0.99; Patient 3 SUV 0.80). No additional upregulation was detected elsewhere at either time point.
Conclusions:
The neuroinflammatory reaction after ischaemic stroke is limited in time and circumscribed in space suggesting that post-ischaemic inflammation is tightly controlled but regulatory mechanisms.
Insights
This study used PET imaging to track brain inflammation after ischemic stroke. Neuroinflammation was detected in the acute phase but resolved by 90 days, indicating a time-limited inflammatory response.
Area of Science:
- Neuroscience
- Radiology
- Immunology
Background:
- Microglial activation plays a dual role in ischemic stroke, contributing to both damage and repair.
- Clinical imaging of post-stroke inflammation is limited due to logistical challenges.
Purpose of the Study:
- To characterize the spatio-temporal profile of brain inflammation after ischemic stroke.
- To utilize 18kD translocator protein (TSPO) positron emission tomography (PET) with MR co-registration.
Main Methods:
- Three patients underwent MRI and [11C]PBR28 PET scans at 15 ± 3 and 90 ± 7 days post-stroke.
- Regions of interest (ROI) were defined on MRI and applied to PET data to derive time-activity curves.
- Standardized uptake values (SUV) quantified tracer binding in the infarct and surrounding brain regions.
Main Results:
- Increased [11C]PBR28 uptake was observed in the infarct area during the subacute phase.
- Tracer uptake returned to baseline levels in non-infarcted areas by 90 days post-stroke.
- No additional inflammation was detected in other brain regions at either time point.
Conclusions:
- The neuroinflammatory response following ischemic stroke is spatially restricted and temporally limited.
- Post-stroke inflammation appears to be tightly regulated by underlying mechanisms.
