Increased peripheral benzodiazepine binding sites in the brain of patients with Huntington's disease
Abstract
Huntington's disease (HD) is a hereditary disorder associated with the development of dyskinesias and dementia, characterised by profound atrophy of the striatum and, to a lesser extent, other brain areas. A relative gliosis has been described. One marker for such inflammatory gliosis is an elevation of peripheral type benzodiazepine binding sites (PTBBS); these have also been shown to be increased following acute experimental and chronic degenerative neuronal damage. The present study investigates [3H]PK11195 binding to PTBBS in three brain areas of HD patients. We found a highly significant increase in PTBBS density in the putamen, a moderate but significant increase in the frontal cortex of HD patients and no significant change in the temporal cortex. Comparing these results to findings in other neurodegenerative diseases, e.g. Alzheimer's disease, where inflammation is discussed as a possible primary as well as a secondary pathological mechanism, our observations point to a possible involvement of inflammation in the neurodegenerative process in HD.
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PET imaging has shown increased TSPO signal in a range of human neurodegenerative diseases with an inflammatory component.
“Accordingly, using PET imaging, increased TSPO signal has been observed in a range of human neurodegenerative diseases with an inflammatory component, such as simian immunodeficiency virus encephalitis [10], multiple sclerosis [11], Huntington’s [12] and Alzheimer’s disease [13].”
From Pharmacological modulation of TSPO in microglia/macrophages and neurons in a chronic neurodegenerative model of prion disease (2023) · cites this paper as [12]
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Microglial activation correlates with severity in Huntington disease: A clinical and PET study
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Cyclic GMP-AMP synthase promotes the inflammatory and autophagy responses in Huntington disease
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A quantitative neuropathological assessment of translocator protein expression in multiple sclerosis
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“…viral encephalitis (Banati et al. , 1999; Cagnin et al. , 2001), amyotrophic lateral sclerosis (Turner et al. , 2004 a ), Huntington’s disease (Meßmer and Reynolds, 1998) and frontotemporal dementia (Cagnin et al. , 2004) and thus has become recognized as a marker of in vivo neuroinflammation…”
Imaging of microglia in patients with neurodegenerative disorders
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Inflammation in transgenic mouse models of neurodegenerative disorders
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The hGFAP-driven conditional TSPO knockout is protective in a mouse model of multiple sclerosis
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“Accordingly, using PET imaging, increased TSPO signal has been observed in a range of human neurodegenerative diseases with an inflammatory component, such as simian immunodeficiency virus encephalitis [10], multiple sclerosis [11], Huntington’s [12] and Alzheimer’s disease [13].”
Background
- Authors
- Meßmer, K., & Reynolds, G. P.
- Affiliations
- University of Sheffield (GB)
- Corresponding author
- Reynolds, Gavin P
- ORCID
- Reynolds, Gavin P
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 1998-01
- Volume
- 241
- Issue
- 1
- Pages
- 53-56
- ISSN
- 0304-3940 (ISSN-L)
- OpenAlex
- W2014079296
- Cited by
- 89
- References
- 1
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2023: 2 · 2020: 2 · 2019: 4 · 2018: 4 · 2017: 3 · 2016: 4 · 2015: 2 · 2014: 6 · 2013: 3 · 2012: 3
- FWCI
- 0.66
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- Huntington's disease, neuroinflammation, gliosis, putamen, frontal cortex, temporal cortex, striatal atrophy, neurodegeneration, Alzheimer's disease comparison
- MeSH terms
- Adult, Aged, Benzodiazepines, Binding Sites, Brain, Frontal Lobe, Humans, Huntington Disease, Middle Aged, Putamen, Radioligand Assay, Temporal Lobe
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