PET Imaging in Huntington's Disease
- PMID: 26683130
- PMCID: PMC4927896
- DOI: 10.3233/JHD-150171
PET Imaging in Huntington's Disease
Abstract
To date, little is known about how neurodegeneration and neuroinflammation propagate in Huntington's disease (HD). Unfortunately, no treatment is available to cure or reverse the progressive decline of function caused by the disease, thus considering HD a fatal disease. Mutation gene carriers typically remain asymptomatic for many years although alterations in the basal ganglia and cortex occur early on in mutant HD gene-carriers. Positron Emission Tomography (PET) is a functional imaging technique of nuclear medicine which enables in vivo visualization of numerous biological molecules expressed in several human tissues. Brain PET is most powerful to study in vivo neuronal and glial cells function as well as cerebral blood flow in a plethora of neurodegenerative disorders including Parkinson's disease, Alzheimer's and HD. In absence of HD-specific biomarkers for monitoring disease progression, previous PET studies in HD were merely focused on the study of dopaminergic terminals, cerebral blood flow and glucose metabolism in manifest and premanifest HD-gene carriers. More recently, research interest has been exploring novel PET targets in HD including the state of phosphodiesterse expression and the role of activated microglia. Hence, a better understanding of the HD pathogenesis mechanisms may lead to the development of targeted therapies. PET imaging follow-up studies with novel selective PET radiotracers such as 11C-IMA-107 and 11C-PBR28 may provide insight on disease progression and identify prognostic biomarkers, elucidate the underlying HD pathology and assess novel pharmaceutical agents and over time.
Keywords: Huntington’s disease; PET; TSPO; cortex; dopaminergic; microglia; putamen; striatum.
Similar articles
-
Huntington's Disease: A Review of the Known PET Imaging Biomarkers and Targeting Radiotracers.Molecules. 2020 Jan 23;25(3):482. doi: 10.3390/molecules25030482. Molecules. 2020. PMID: 31979301 Free PMC article. Review.
-
Neuroinflammation in Huntington's Disease: New Insights with 11C-PBR28 PET/MRI.ACS Chem Neurosci. 2018 Nov 21;9(11):2563-2571. doi: 10.1021/acschemneuro.8b00072. Epub 2018 May 17. ACS Chem Neurosci. 2018. PMID: 29719953
-
Current status of PET imaging in Huntington's disease.Eur J Nucl Med Mol Imaging. 2016 Jun;43(6):1171-82. doi: 10.1007/s00259-016-3324-6. Epub 2016 Feb 22. Eur J Nucl Med Mol Imaging. 2016. PMID: 26899245 Free PMC article. Review.
-
Molecular Imaging in Huntington's Disease.Int Rev Neurobiol. 2018;142:289-333. doi: 10.1016/bs.irn.2018.08.007. Epub 2018 Aug 29. Int Rev Neurobiol. 2018. PMID: 30409256 Review.
-
Cortical atrophic-hypometabolic dissociation in the transition from premanifest to early-stage Huntington's disease.Eur J Nucl Med Mol Imaging. 2019 May;46(5):1111-1116. doi: 10.1007/s00259-018-4257-z. Epub 2019 Jan 9. Eur J Nucl Med Mol Imaging. 2019. PMID: 30627816
Cited by
-
Neuroimaging of Mouse Models of Alzheimer's Disease.Biomedicines. 2022 Jan 28;10(2):305. doi: 10.3390/biomedicines10020305. Biomedicines. 2022. PMID: 35203515 Free PMC article. Review.
-
An unusual presentation of Huntington's disease.Clin Case Rep. 2021 Jul 16;9(7):e04547. doi: 10.1002/ccr3.4547. eCollection 2021 Jul. Clin Case Rep. 2021. PMID: 34295499 Free PMC article.
-
A PET-CT study on neuroinflammation in Huntington's disease patients participating in a randomized trial with laquinimod.Brain Commun. 2023 Apr 3;5(2):fcad084. doi: 10.1093/braincomms/fcad084. eCollection 2023. Brain Commun. 2023. PMID: 37020532 Free PMC article.
-
Huntington's Disease Presenting as Adult-Onset Parkinsonism.J Clin Neurol. 2022 Jan;18(1):87-89. doi: 10.3988/jcn.2022.18.1.87. J Clin Neurol. 2022. PMID: 35021281 Free PMC article. No abstract available.
-
Huntington's Disease: A Review of the Known PET Imaging Biomarkers and Targeting Radiotracers.Molecules. 2020 Jan 23;25(3):482. doi: 10.3390/molecules25030482. Molecules. 2020. PMID: 31979301 Free PMC article. Review.
References
-
- Turjanski N, Weeks R, Dolan R, Harding AE, Brooks DJ. Striatal D1 and D2 receptor binding in patients withHuntington’s disease and other choreas. A PET study. Brain. 1995;118(3):689–96. - PubMed
-
- Weeks RA, Piccini P, Harding AE, Brooks DJ. Striatal D1 and D2 dopamine receptor loss in asymptomatic mutation carriers of Huntington’s disease. Ann Neurol. 1996;40(1):49–54. - PubMed
-
- Antonini A, Leenders KL, Spiegel R, Meier D, Vontobel P, Weigell-Weber M, et al. Striatal glucose metabolism and dopamine D2 receptor binding in asymptomatic gene carriers and patients with Huntington’s disease. Brain. 1996;119(6):2085–95. - PubMed
-
- Antonini A, Leenders KL, Eidelberg D. [11C]raclopride-PET studies of the Huntington’s disease rate of progression: Relevance of the trinucleotide repeat length. Ann Neurol. 1998;43(2):253–5. - PubMed
-
- Pavese N, Andrews TC, Brooks DJ, Ho AK, Rosser AE, Barker RA, et al. Progressive striatal and cortical dopamine receptor dysfunction in Huntington’s disease: A PET study. Brain. 2003;126(11):1127–35. - PubMed
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Medical