Publications by authors named "Laura Saari"

4 Publications

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Depression and Nigral Neuron Density in Lewy Body Spectrum Diseases.

Ann Neurol 2021 May 3;89(5):1046-1050. Epub 2021 Mar 3.

Clinical Neurosciences, University of Turku, Turku, Finland.

Parkinson's disease and other Lewy body spectrum diseases (LBDs) are associated with a specific risk for clinical depression. In the present clinicopathological study with 73 patients with LBD, we observed that the substantia nigra pars compacta dopamine neuron density was markedly lower in patients who had comorbid depression antemortem than in nondepressed patients (1.52 vs 2.32 n/mm , p = 0.004). There were no differences in cognition, motor disease severity, antiparkinsonian medications, or disease duration between groups. The results implicate the substantia nigra as an important psychomotor modulatory area of mood in patients with Lewy body disorders. ANN NEUROL 2021;;89:1046-1050.
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http://dx.doi.org/10.1002/ana.26046DOI Listing
May 2021

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

Mov Disord 2019 10 24;34(10):1562-1566. Epub 2019 Jun 24.

Department of Neurology, University of Turku, Turku, Finland.

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.
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http://dx.doi.org/10.1002/mds.27777DOI Listing
October 2019

Dopamine transporter imaging does not predict the number of nigral neurons in Parkinson disease.

Neurology 2017 Apr 10;88(15):1461-1467. Epub 2017 Mar 10.

From the Division of Clinical Neurosciences (L.S., J.J., V.K.), Turku University Hospital, Turku, Finland; Department of Neurology (L.S., J.J., V.K.) and Turku PET Centre (J.J., T.N., V.K.), University of Turku; and Departments of Pathology (K.K., M.G.) and Clinical Physiology and Nuclear Medicine (T.N.), Turku University Hospital and University of Turku, Finland.

Objective: To examine possible associations between in vivo brain dopamine transporter SPECT imaging and substantia nigra pars compacta (SNc) neuronal survival in Parkinson disease (PD).

Methods: Nigral neuron numbers were calculated for 18 patients (11 patients with neuropathologically confirmed PD) who had been examined with dopamine transporter (DAT) SPECT before death. Correlation analyses between SNc tyrosine hydroxylase (TH)-positive and neuromelanin-containing neuron counts and DAT striatal specific binding ratios (SBRs) were performed with semiquantitative region of interest-based and voxel-based analyses.

Results: Mean putamen SBR did not correlate with the number of substantia nigra TH-positive ( = -0.11, = 0.66) or neuromelanin-containing ( = -0.07, = 0.78) neurons. Correlations remained clearly nonsignificant when the time interval between SPECT and death was used as a covariate, when the voxel-based analysis was used, and when only patients with PD were included.

Conclusions: This cohort study demonstrates that postmortem SNc neuron counts are not associated with striatal DAT binding in PD. These results fit with the theory that there is no correlation between the number of substantia nigra neurons and striatal dopamine after a certain level of damage has occurred. Striatal DAT binding in PD may reflect axonal dysfunction or DAT expression rather than the number of viable neurons.
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http://dx.doi.org/10.1212/WNL.0000000000003810DOI Listing
April 2017