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Updated: Jul 16, 2026
In Vivo Dynamics of Retinal Microglial Activation During Neurodegeneration: Confocal Ophthalmoscopic Imaging and Cell Morphometry in Mouse Glaucoma
Published on: May 11, 2015
Imaging microglial activation in Huntington's disease
Yen F Tai1, Nicola Pavese, Alexander Gerhard
1Division of Neuroscience and Psychological Medicine, Hammersmith Hospital, Imperial College London, UK.
Abstract:
Activated microglia have been proposed to play a major role in the pathogenesis of Huntington's Disease (HD). PK11195 is a ligand which binds selectively to peripheral benzodiazepine binding sites, a type of receptor selectively expressed by activated microglia in the central nervous system. Using (11)C-(R)-PK11195 positron emission tomography (PET), we have recently shown in vivo evidence of increased microglial activation in both symptomatic and presymptomatic HD gene carriers and that the degree of microglial activation in the striatum correlates with the severity of striatal dopamine D2 receptor dysfunction measured with (11)C-raclopride PET. Our findings indicate that microglial activation is an early process in the HD pathology, occurring before the onset of symptoms. The close spatial and temporal relationship between microglial activation and neuronal dysfunction lends further support to the pathogenic link between the two processes in HD. Further longitudinal studies are needed to fully elucidate this link.
Insights
Microglial activation, a marker of brain inflammation, is an early process in Huntington's Disease (HD). This occurs even before symptoms appear, suggesting a key role in HD pathogenesis.
Area of Science:
- Neuroscience
- Neuroinflammation
- Molecular Imaging
Background:
- Activated microglia are implicated in Huntington's Disease (HD) pathogenesis.
- PK11195 is a ligand for peripheral benzodiazepine binding sites on activated microglia.
- Microglial activation is a potential early biomarker in HD.
Purpose of the Study:
- To investigate in vivo microglial activation in HD patients and gene carriers.
- To correlate microglial activation with striatal dopamine D2 receptor dysfunction.
- To establish microglial activation as an early pathological event in HD.
Main Methods:
- Positron Emission Tomography (PET) imaging using (11)C-(R)-PK11195.
- Assessment of microglial activation in symptomatic and presymptomatic HD gene carriers.
- Correlation analysis with (11)C-raclopride PET measurements of striatal dopamine D2 receptor function.
Main Results:
- Increased microglial activation was observed in both symptomatic and presymptomatic HD gene carriers.
- Microglial activation in the striatum correlated with dopamine D2 receptor dysfunction severity.
- Microglial activation precedes symptom onset in HD.
Conclusions:
- Microglial activation is an early pathological process in Huntington's Disease.
- A link exists between microglial activation and neuronal dysfunction in HD.
- Further longitudinal studies are required to fully understand this link.
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