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Mov Disord. 2014 Aug;29(9):1197-201. doi: 10.1002/mds.25893. Epub 2014 May 5.

In vivo dopaminergic and serotonergic dysfunction in DCTN1 gene mutation carriers.

Author information

1
Pacific Parkinson's Research Centre, University of British Columbia, Vancouver, BC, Canada.

Abstract

INTRODUCTION:

We used positron emission tomography (PET) to assess dopaminergic and serotonergic terminal density in three subjects carrying a mutation in the DCT1 gene, two clinically affected with Perry syndrome.

METHODS:

All subjects had brain imaging using 18F-6-fluoro-l-dopa (FDOPA, dopamine synthesis and storage), (+)-11C-dihydrotetrabenazine (DTBZ, vesicular monoamine transporter type 2), and 11C-raclopride (RAC, dopamine D2/D3 receptors). One subject also underwent PET with 11C-3-amino-4-(2-dimethylaminomethyl-phenylsulfanyl)-benzonitrile (DASB, serotonin transporter).

RESULTS:

FDOPA-PET and DTBZ-PET in the affected individuals showed a reduction of striatal tracer uptake. Also, RAC-PET showed higher uptake in these area. DASB-PET showed significant uptake changes in left orbitofrontal cortex, bilateral anterior insula, left dorsolateral prefrontal cortex, left orbitofrontal cortex, left posterior cingulate cortex, left caudate, and left ventral striatum.

CONCLUSIONS:

Our data showed evidence of both striatal dopaminergic and widespread cortical/subcortical serotonergic dysfunctions in individuals carrying a mutation in the DCTN1 gene.

KEYWORDS:

Perry syndrome; dopaminergic dysfunction; dynactin gene; positron emission tomography; serotonergic dysfunction

PMID:
24797316
PMCID:
PMC4139463
DOI:
10.1002/mds.25893
[Indexed for MEDLINE]
Free PMC Article

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