Literature DB >> 26802091

Change in PDE10 across early Huntington disease assessed by [18F]MNI-659 and PET imaging.

David S Russell1, Danna L Jennings2, Olivier Barret2, Gilles D Tamagnan2, Vincent M Carroll2, Fabien Caillé2, David Alagille2, Thomas J Morley2, Caroline Papin2, John P Seibyl2, Kenneth L Marek2.   

Abstract

OBJECTIVE: To evaluate whether striatal [(18)F]MNI-659 PET imaging of phosphodiesterase 10A (PDE10) serves as a sensitive and reliable biomarker of striatal neurodegeneration in a longitudinal cohort of participants with early Huntington disease (HD).
METHODS: A cohort of participants with HD, including both participants premanifest or manifest with motor signs, underwent clinical assessments, genetic determination, and 2 [(18)F]MNI-659 PET imaging sessions approximately 1 year apart. Eleven healthy control (HC) participants underwent clinical assessments and [(18)F]MNI-659 PET imaging once. Striatal binding potentials (BPnd) were estimated for brain regions of interest, specifically within the basal ganglia, and compared between baseline and follow-up imaging. Clinical measures of HD severity were assessed at each visit.
RESULTS: Eight participants with HD (6 manifest; 2 premanifest) participated. Of those with manifest HD, all had relatively early stage disease (stage 1, n = 2; stage 2, n = 4) and a Unified Huntington's Disease Rating Scale total motor score <45. As expected, the HD cohort as a whole had a reduction in the basal ganglia BPnd to approximately 50% of that seen in HC. On follow-up scans, [(18)F]MNI-659 uptake declined in the putamen and caudate nucleus in all 8 participants. The mean annualized rates of decline in signal in the caudate, putamen, and globus pallidus and the putamen were 16.6%, 6.9%, and 5.8%, respectively. In HC, the annualized reduction in signal in striatal regions was less than 1%.
CONCLUSION: Longitudinal data in this small cohort of participants with early HD support [(18)F]MNI-659 PET imaging of PDE10 as a useful biomarker to track HD disease progression.
© 2016 American Academy of Neurology.

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Year:  2016        PMID: 26802091     DOI: 10.1212/WNL.0000000000002391

Source DB:  PubMed          Journal:  Neurology        ISSN: 0028-3878            Impact factor:   9.910


  22 in total

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3.  Allele-selective transcriptional repression of mutant HTT for the treatment of Huntington's disease.

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4.  Synaptic Vesicle Glycoprotein 2A Is Affected in the Central Nervous System of Mice with Huntington Disease and in the Brain of a Human with Huntington Disease Postmortem.

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6.  Phosphodiesterases PDE2A and PDE10A both change mRNA expression in the human brain with age, but only PDE2A changes in a region-specific manner with psychiatric disease.

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Review 7.  Therapeutic targeting of 3',5'-cyclic nucleotide phosphodiesterases: inhibition and beyond.

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Review 9.  Molecular Imaging Markers to Track Huntington's Disease Pathology.

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