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Microglial activation correlates with severity in Huntington disease: A clinical and PET study
Abstract
BACKGROUND: Huntington disease (HD) is characterized by the progressive death of medium spiny dopamine receptor bearing striatal GABAergic neurons. In addition, microglial activation in the areas of neuronal loss has recently been described in postmortem studies. Activated microglia are known to release neurotoxic cytokines, and these may contribute to the pathologic process. METHODS: To evaluate in vivo the involvement of microglia activation in HD, the authors studied patients at different stages of the disease using [(11)C](R)-PK11195 PET, a marker of microglia activation, and [(11)C]raclopride PET, a marker of dopamine D2 receptor binding and hence striatal GABAergic cell function. RESULTS: In HD patients, a significant increase in striatal [(11)C](R)-PK11195 binding was observed, which significantly correlated with disease severity as reflected by the striatal reduction in [(11)C]raclopride binding, the Unified Huntington's Disease Rating Scale score, and the patients' CAG index. Also detected were significant increases in microglia activation in cortical regions including prefrontal cortex and anterior cingulate. CONCLUSIONS: These [(11)C](R)-PK11195 PET findings show that the level of microglial activation correlates with Huntington disease (HD) severity. They lend support to the view that microglia contribute to the ongoing neuronal degeneration in HD and indicate that [(11)C](R)-PK11195 PET provides a valuable marker when monitoring the efficacy of putative neuroprotecting agents in this relentlessly progressive genetic disorder.
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“Huntington's disease is associated with a reactive microglial response and consequent inflammation.”
From Microglial depletion prevents extracellular matrix changes and striatal volume reduction in a model of Huntington's disease (2020) · cites this paper as Pavese et al., 2006
In the citing paper
“In Huntington's disease, microglial activation is detected years before the onset of clinical symptoms and correlates with striatal neuron dysfunction in subclinical (Tai et al. , 2007) as well as clinical stages of the disease (Pavese et al. , 2006; Politis et al. , 2011).”
From Microglial depletion prevents extracellular matrix changes and striatal volume reduction in a model of Huntington's disease (2020) · cites this paper as Pavese et al., 2006
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“Microglia, a cellular indicator of inflammation, is also increased in the striatum of HD animal and cell culture models and HD patients (12-14).”
BackgroundTSPO’nun (18 kDa Translokatör Protein) Yapısı, İşlevi ve Patolojik Süreçlerdeki Rolü
Elma, Y., & Can, E. Y. (2024) · Medical Journal of Western Black Sea · doi:10.29058/mjwbs.1477979 · Cited by 1
Dysregulation of miRNAs in Sicilian Patients with Huntington’s Disease
Salemi, M., Schillaci, F. A., Salluzzo, M. G., Marchese, G., Ventola, G. M., Perrotta, C. S., Stefano, V. D., Lanza, G., & Ferri, R. (2025) · Diagnostics · doi:10.3390/diagnostics15192454 · Cited by 1
“Pro-inflammatory activation of microglia is detectable in HD patients or even at a pre-symptomatic stage [55,56], suggesting that it might be an early event in the pathogenesis of HD; moreover, it correlates with disease progression [57].”
Kong, W., Jiang, J., Wang, Y., Chen, J., Wang, B., Wang, K., Liang, Y., Wang, J., Li, C., Lin, Y., et al. (2026) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2026.1780056 · Cited by 3
“This also disrupts the metabolism and balance of key neurotransmitters like dopamine and acetylcholine (43, 44), contributing to POD.”
Therapeutic Approach in Huntington's Disease
Dürr, A. (2008) · Handbook of clinical neurology · doi:10.1016/s0072-9752(07)01258-4 · Cited by 1
“The role of anti-in flammator y agents in slowi ng down the progression of HD could be tested, since microglial activation early in the disease has been noticed (Pavese et al., 2006).”
BackgroundBiomarkers for Huntington’s Disease
Kobal, J., Lovrei, L., & Peterli, B. (2012) · InTech eBooks · doi:10.5772/32757 · Cited by 1
“…D2 receptor binding of 5-6 per cent in HD patients and of around 4 per cent in premanifest HD gene carriers (Pavese et al 2003) Microglial activation was observed in the striatum of both HD patients and presymptomatic HD gene carriers by reduced binding of 11C-raclopride (Pavese et al 2006).”
BackgroundWoodcock, T. (2010) · UKnowledge (University of Kentucky) · Cited by 1
Functional imaging in Huntington disease
Niethammer, M., & Eidelberg, D. (2017) · Handbook of clinical neurology · doi:10.1016/b978-0-12-801893-4.00021-3 · Cited by 1
Plant Metabolites and More Treating Various Ailments
Badal, S. A. M. (2016) · Elsevier eBooks · doi:10.1016/b978-0-12-802104-0.00016-0 · Cited by 1
Neurotoxicity in Huntington Disease
Loy, C. T., & Hannan, A. J. (2014) · Springer eBooks · doi:10.1007/978-1-4614-5836-4_140 · Cited by 1
Jankovic, J. J., Hallett, M., Okun, M. S., Comella, C., Fahn, S., & Goldman, J. G. (2021) · Elsevier eBooks · doi:10.1016/b978-0-323-31071-0.00013-5 · Cited by 1
Goyal, A., Gopika, S., & Agrawal, N. (2022) · Protein and Peptide Letters · doi:10.2174/0929866529666220622124253 · Cited by 1
Pais, M. L., Jorge, L., Martins, R., Canário, N., Xavier, A. C., Bernardes, R., Abrunhosa, A., Santana, I. J., & Castelo-Branco, M. S. (2023) · Brain Communications · doi:10.1093/braincomms/fcad148 · Cited by 1
Inflammation Biomarkers in Huntington’s Disease
Björkqvist, M. (2023) · Contemporary clinical neuroscience · doi:10.1007/978-3-031-32815-2_11 · Cited by 1
Altered Metabolic Signaling and Potential Therapies in Polyglutamine Diseases
Vohra, A., Keefe, P., & Puthanveetil, P. (2024) · Metabolites · doi:10.3390/metabo14060320 · Cited by 1
“The extent of reactive microglial presence has been linked to the severity of the disease and often occurs alongside proteasome activation and in the excess production of free radicals [149].”
BackgroundPET Imaging of Microglia Activation in Neuropsychiatric Disorders with Potential Infectious Origin
Klein, H. C., de Witte, L. D., Bransfield, R. C., & Deyn, P. P. D. (2014) · Springer eBooks · doi:10.1007/978-3-642-54307-4_34 · Cited by 1
Huntington Disease, Parkinson Disease, and Other Neurodegenerative Diseases
Möller, T. (2012) · Oxford University Press eBooks · doi:10.1093/med/9780199794591.003.0065 · Cited by 1
Klein, H. C., de Witte, L. D., Bransfield, R. C., & Deyn, P. P. D. (2020) · Springer eBooks · doi:10.1007/978-3-030-53168-3_32 · Cited by 1
Zamora, C. A., Muhleman, M., & Castillo, M. (2021) · Springer eBooks · doi:10.1007/978-3-030-82367-2_35 · Cited by 1
Kremer, H. (2020) · Springer eBooks · doi:10.1007/978-3-030-53168-3_28 · Cited by 1
Neuroimaging Biomarkers for Huntington’s Disease
van de Zande, N. A., Ghariq, E., de Bresser, J., & de Bot, S. T. (2022) · IntechOpen eBooks · doi:10.5772/intechopen.102528 · Cited by 1
de Natale, E. R., Wilson, H., Udeh‐Momoh, C. T., Ford, J. K., Politis, M., & Middleton, L. T. (2022) · Elsevier eBooks · doi:10.1016/b978-0-12-823761-8.00022-7 · Cited by 1
Metadata
- Authors
- Pavese, N., Gerhard, A., Tai, Y. F., Ho, A. K., Turkheimer, F., Barker, R. A., Brooks, D. J., & Piccini, P.
- Affiliations
- Hammersmith Hospital (GB)
- Venue
- Neurology
- Published
- 2006-06-13
- Volume
- 66
- Issue
- 11
- Pages
- 1638-1643
- ISSN
- 0028-3878 (ISSN-L)
- 1526-632X
- OpenAlex
- W2025681964
- Cited by
- 462
- References
- 35
- Citations by year
- 2026: 12 · 2025: 19 · 2024: 30 · 2023: 26 · 2022: 22 · 2021: 26 · 2020: 27 · 2019: 19 · 2018: 18 · 2017: 31 · 2016: 25 · 2015: 25 · 2014: 38 · 2013: 19 · 2012: 14
- FWCI
- 8.08
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neurology (publishedVersion)
- PubMed (publishedVersion)
- CentAUR (University of Reading) (acceptedVersion)
- Research Explorer (The University of Manchester) (submittedVersion)
- Funders
- Wellcome Trust
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological diseases and metabolism
- Keywords
- Huntington's disease, microglial activation, dopamine D2 receptor binding, disease severity, neuroinflammation, neurodegeneration, prefrontal cortex, anterior cingulate cortex, CAG repeat expansion
- MeSH terms
- Adult, Aged, Amides, Corpus Striatum, Female, Humans, Huntington Disease, Isoquinolines, Male, Middle Aged, Sensitivity and Specificity, Severity of Illness Index, Statistics as Topic, Reproducibility of Results, Microglia, Radiopharmaceuticals, Raclopride, Positron-Emission Tomography
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