Skip to main page content
U.S. flag

An official website of the United States government

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2015;4(4):287-96.
doi: 10.3233/JHD-150171.

PET Imaging in Huntington's Disease

Free PMC article
Review

PET Imaging in Huntington's Disease

Andreas-Antonios Roussakis et al. J Huntingtons Dis. 2015.
Free PMC article

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.

PubMed Disclaimer

Similar articles

Cited by

References

    1. 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
    1. 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
    1. 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
    1. 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
    1. 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

Substances