No link between striatal dopaminergic axons and dopamine transporter imaging in Parkinson's disease.


Journal

Movement disorders : official journal of the Movement Disorder Society
ISSN: 1531-8257
Titre abrégé: Mov Disord
Pays: United States
ID NLM: 8610688

Informations de publication

Date de publication:
10 2019
Historique:
received: 14 03 2019
revised: 29 05 2019
accepted: 31 05 2019
pubmed: 25 6 2019
medline: 13 6 2020
entrez: 25 6 2019
Statut: ppublish

Résumé

Brain dopamine transporter binding has been considered a possible biomarker for nigrostriatal degeneration in PD. To investigate whether dopamine transporter binding is associated with the number of dopaminergic neurites in the putamen. Tyrosine hydroxylase-positive nerve fibers were counted from postmortem putamen sections taken from 14 parkinsonism patients who had been scanned with dopamine transporter single-photon emission computed tomography antemortem. Fiber counts were correlated with putamen dopamine transporter binding and SN neuron counts. The putamen dopamine transporter specific binding ratio did not correlate with the putamen tyrosine hydroxylase-positive axon counts (r = 0.00; P = 1.0; PD patients: r = 0.07; P = 0.86). The nigra neuron counts had a positive correlation with the putamen tyrosine hydroxylase-positive axon counts. Striatal dopamine transporter imaging does not associate with axonal nor somal loss of the nigrostriatal neurons in PD. It may reflect dopaminergic activity rather than number of surviving neurons or their striatal projection axons. © 2019 International Parkinson and Movement Disorder Society.

Sections du résumé

BACKGROUND
Brain dopamine transporter binding has been considered a possible biomarker for nigrostriatal degeneration in PD.
OBJECTIVE
To investigate whether dopamine transporter binding is associated with the number of dopaminergic neurites in the putamen.
METHODS
Tyrosine hydroxylase-positive nerve fibers were counted from postmortem putamen sections taken from 14 parkinsonism patients who had been scanned with dopamine transporter single-photon emission computed tomography antemortem. Fiber counts were correlated with putamen dopamine transporter binding and SN neuron counts.
RESULTS
The putamen dopamine transporter specific binding ratio did not correlate with the putamen tyrosine hydroxylase-positive axon counts (r = 0.00; P = 1.0; PD patients: r = 0.07; P = 0.86). The nigra neuron counts had a positive correlation with the putamen tyrosine hydroxylase-positive axon counts.
CONCLUSIONS
Striatal dopamine transporter imaging does not associate with axonal nor somal loss of the nigrostriatal neurons in PD. It may reflect dopaminergic activity rather than number of surviving neurons or their striatal projection axons. © 2019 International Parkinson and Movement Disorder Society.

Identifiants

pubmed: 31234224
doi: 10.1002/mds.27777
doi:

Substances chimiques

Dopamine Plasma Membrane Transport Proteins 0
SLC6A3 protein, human 0
Dopamine VTD58H1Z2X

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1562-1566

Commentaires et corrections

Type : CommentIn
Type : CommentIn

Informations de copyright

© 2019 International Parkinson and Movement Disorder Society.

Références

Tagliaferro P, Burke RE. Retrograde axonal degeneration in Parkinson disease. J Parkinsons Dis 2016;6:1-15.
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Fazio P, Svenningsson P, Cselényi Z, Halldin C, Farde L, Varrone A. Nigrostriatal dopamine transporter availability in early Parkinson's disease. Mov Disord 2018;33:592-599.
Saari L, Kivinen K, Gardberg M, Joutsa J, Noponen T, Kaasinen V. Dopamine transporter imaging does not predict the number of nigral neurons in Parkinson disease. Neurology 2017;88:1461-1467.
Jankovic J. Parkinson's disease tremors and serotonin. Brain 2018;141:624-626.
Joutsa J, Gardberg M, Röyttä M, Kaasinen V. Diagnostic accuracy of parkinsonism syndromes by general neurologists. Parkinsonsim Relat Disord 2014;20:840-844.
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Auteurs

Emma A Honkanen (EA)

Department of Neurology, University of Turku, Turku, Finland.
Division of Clinical Neurosciences, Turku University Hospital, Turku, Finland.

Laura Saari (L)

Department of Neurology, University of Turku, Turku, Finland.
Division of Clinical Neurosciences, Turku University Hospital, Turku, Finland.

Katri Orte (K)

Department of Pathology, Institute of Biomedicine, University of Turku and Turku University Hospital, Turku, Finland.

Maria Gardberg (M)

Department of Pathology, Institute of Biomedicine, University of Turku and Turku University Hospital, Turku, Finland.

Tommi Noponen (T)

Department of Clinical Physiology and Nuclear Medicine, Turku University Hospital, Turku, Finland.
Department of Medical Physics, Turku University Hospital, Turku, Finland.

Juho Joutsa (J)

Department of Neurology, University of Turku, Turku, Finland.
Division of Clinical Neurosciences, Turku University Hospital, Turku, Finland.
Turku Brain and Mind Center, University of Turku, Turku, Finland.

Valtteri Kaasinen (V)

Department of Neurology, University of Turku, Turku, Finland.
Division of Clinical Neurosciences, Turku University Hospital, Turku, Finland.

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