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Microglia Activation in Basal Ganglia Is a Late Event in Huntington Disease Pathophysiology
Open accessAbstract
OBJECTIVE: To define the role played by microglia in different stages of Huntington disease (HD), we used the TSPO radioligand [11C]-ER176 and PET to evaluate microglial activation in relation to neurodegeneration and in relation to the clinical features seen at premanifest and manifest stages of the disease. METHODS: This is a cross-sectional study in which 18 subjects (6 controls, 6 premanifest, and 6 manifest HD gene carriers) underwent a [11C]-ER176 PET scan and an MRI for anatomic localization. Segmentation of regions of interest (ROIs) was performed, and group differences in [11C]-ER176 binding (used to evaluate the extent of microglial activation) were assessed by the standardized uptake value ratio (SUVR). Microglial activation was correlated with ROIs volumes, disease burden, and the scores obtained in the clinical scales. As an exploratory aim, we evaluated the dynamic functions of microglia in vitro, by using induced microglia-like (iMG) cells from peripheral blood monocytes. RESULTS: Individuals with manifest HD present higher [11C]-ER176 SUVR in both globi pallidi and putamina in comparison with controls. No differences were observed when we compared premanifest HD with controls or with manifest HD. We also found a significant correlation between increased microglial activation and cumulative disease burden, and with reduced volumes. iMG from controls, premanifest HD, and manifest HD patients showed similar phagocytic capacity. CONCLUSIONS: Altogether, our data demonstrate that microglial activation is involved in HD pathophysiology and is associated with disease progression.
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Neuroinflammation and microglial activation are consistent features across neurodegenerative diseases, including AD, PD, HD, FTD, and ALS.
“Indeed, neuroinflammation and microglial activation are consistent features across neurodegenerative diseases, including AD,126–128 PD,86,129 HD,130,131 FTD,91,132 and ALS.89,133–135”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [130]
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Bonilla-Vidal, L., Esteruelas, G., Ettcheto, M., Gomara, M. J., Haro, I., Souto, E. B., Espina, M., Camins, A., García, M. L., Cano, A. C., et al. (2023) · Springer eBooks · doi:10.1007/978-981-99-6807-7_18
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Targeting redox imbalance and inflammatory cascades in the pathogenesis of neurodegeneration
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Metadata
- Authors
- Rocha, N. P., Charron, O., Latham, L. B., Colpo, G. D., Zanotti-Fregonara, P., Yu, M., Freeman, L., Furr Stimming, E., & Teixeira, A. L.
- Affiliations
- From the Mitchell Center for Alzheimer's Disease and Related Brain Disorders (N.P.R.), Department of Neurology, McGovern Medical School, The University of Texas Health Science Center, Houston; Department of Neurology (O.C., L.F.), The University of Texas at Austin; School of Medicine (L.B.L.), University of Washington, Seattle; Neuropsychiatry Program (G.D.C., A.L.T.), Department of Psychiatry and Behavioral Sciences, McGovern Medical School, University of Texas, Houston; Houston Methodist Research...
- University of Washington (US)
- Venue
- Neurology Neuroimmunology & Neuroinflammation
- Published
- 2021-05
- Volume
- 8
- Issue
- 3
- ISSN
- 2332-7812 (ISSN-L)
- PMC
- PMC8017723
- OpenAlex
- W3148529979
- Cited by
- 52
- References
- 46
- Citations by year
- 2026: 3 · 2025: 9 · 2024: 9 · 2023: 13 · 2022: 15 · 2021: 3
- FWCI
- 4.10
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc-nd
- Locations
- Neurology Neuroimmunology & Neuroinflammation (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- University of Texas Health Science Center at Houston
- McGovern Medical School
- Houston Methodist Research Institute
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Life Sciences › Neuroscience › Neurology › Neurological diseases and metabolism
- Keywords
- Huntington's disease, microglial activation, basal ganglia, TSPO PET, premanifest Huntington disease, globus pallidus, putamen, neurodegeneration, disease progression, phagocytic capacity, neuroinflammation
- MeSH terms
- Adult, Aged, Aged, 80 and over, Basal Ganglia, Brain, Cross-Sectional Studies, Female, Humans, Huntington Disease, Leukocytes, Mononuclear, Male, Middle Aged, Putamen, Microglia, Receptors, GABA, Disease Progression, Positron-Emission Tomography, Primary Cell Culture
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