Measurement of the dopaminergic degeneration in Parkinson’s disease with [123I]β-CIT and SPECT

Brücke, Thomas; Asenbaum, S.; Pirker, Walter; Djamshidian, Schiva; Wenger, S.; Wöber, Christian; Müller, Ch.; Podreka, I.

doi:10.1007/978-3-7091-6842-4_2

Cited by 147 publications

(17 citation statements)

References 44 publications

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“…The P-CIT SPECT of the DRD patient is shown in Fig. 1 compared with (16) is added to show the difference of P-CIT binding with reduced uptake in posterior parts of the striatum.…”

Section: Resultsmentioning

confidence: 99%

[¹²³I]β‐CIT single‐photon emission tomography in DOPA‐responsive dystonia

et al. 1997

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The radiotracer [123I]beta-CIT is a sensitive marker of dopamine uptake sites that can be used to visualize dopaminergic nerve endings in vivo in the human brain. We report on [123I]beta-CIT single-photon emission computed tomography (SPECT) findings in a patient with DOPA-responsive dystonia (DRD). [123I]beta-CIT SPECT showed a striatal radiotracer uptake in the upper range of normal, indicating intact dopamine transporters and structural integrity of nigrostriatal neurons. This differentiates DRD from clinically similar cases with juvenile-onset parkinsonism with dystonia that have a considerable poorer prognosis. [123I]-beta-CIT SPECT may provide a method equally as useful as fluorodopa positron emission tomography in DRD.

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“…The P-CIT SPECT of the DRD patient is shown in Fig. 1 compared with (16) is added to show the difference of P-CIT binding with reduced uptake in posterior parts of the striatum.…”

Section: Resultsmentioning

confidence: 99%

[¹²³I]β‐CIT single‐photon emission tomography in DOPA‐responsive dystonia

et al. 1997

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“…Normal DAT binding using 123 I-FP-CIT appears as two intense symmetric ‘comma-shaped’ regions of activity in the striatum (caudate anteriorly and putamen posteriorly); whereas, an abnormal scan may fall into one of four types: (a) asymmetrically reduced putaminal activity, (b) symmetrically reduced putaminal activity with relative preservation of caudate activity, (c) virtual absence of putaminal activity associated with reduced caudate activity unilaterally or bilaterally, and (d) fairly uniform involvement of putamen and caudate unilaterally or bilaterally [102, 103]. SPECT shows normal density of presynaptic DAT in healthy controls, patients with essential tremor and in drug-induced or psychogenic parkinsonism [104–106], whereas reduced DAT uptake is indicative of nigrostriatal degeneration and is detected in PD, PDD, MSA and PSP patients versus controls [105, 107, 108]. DAT binding was also significantly impaired in DLB and PD patients versus AD and controls [109, 110].…”

Section: Single Photon Emission Computed Tomography In Parkinsonian Dmentioning

confidence: 99%

“…The posterior putamen shows earlier and more severe signal loss than the anterior putamen or caudate in PD [111]. Significant correlations of striatal DAT-SPECT binding with the Hoehn & Yahr disease stage, UPDRS motor score, and with the UPDRS bradykinesia subscale have been demonstrated, although no associations with rigidity or tremor were observed [104, 112–114]. …”

Section: Single Photon Emission Computed Tomography In Parkinsonian Dmentioning

confidence: 99%

“…In contrast to PD and MSA- P , a more symmetric pattern of DAT loss was observed [104, 118, 119], with an index of asymmetry significantly higher in PD than in PSP [119]. Lower striatal-to-occipital, but higher putamen-to-caudate binding ratios were found in PSP versus PD [118, 119], indicating a relatively uniform involvement of striatal dopamine neurons in PSP.…”

Section: Single Photon Emission Computed Tomography In Parkinsonian Dmentioning

confidence: 99%

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Imaging biomarkers in Parkinson’s disease and Parkinsonian syndromes: current and emerging concepts

Saeed

Compagnone

Aviv

et al. 2017

Transl Neurodegener

184

154

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Two centuries ago in 1817, James Parkinson provided the first medical description of Parkinson’s disease, later refined by Jean-Martin Charcot in the mid-to-late 19th century to include the atypical parkinsonian variants (also termed, Parkinson-plus syndromes). Today, Parkinson’s disease represents the second most common neurodegenerative disorder with an estimated global prevalence of over 10 million. Conversely, atypical parkinsonian syndromes encompass a group of relatively heterogeneous disorders that may share some clinical features with Parkinson’s disease, but are uncommon distinct clinicopathological diseases. Decades of scientific advancements have vastly improved our understanding of these disorders, including improvements in in vivo imaging for biomarker identification. Multimodal imaging for the visualization of structural and functional brain changes is especially important, as it allows a ‘window’ into the underlying pathophysiological abnormalities. In this article, we first present an overview of the cardinal clinical and neuropathological features of, 1) synucleinopathies: Parkinson’s disease and other Lewy body spectrum disorders, as well as multiple system atrophy, and 2) tauopathies: progressive supranuclear palsy, and corticobasal degeneration. A comprehensive presentation of well-established and emerging imaging biomarkers for each disorder are then discussed. Biomarkers for the following imaging modalities are reviewed: 1) structural magnetic resonance imaging (MRI) using T1, T2, and susceptibility-weighted sequences for volumetric and voxel-based morphometric analyses, as well as MRI derived visual signatures, 2) diffusion tensor MRI for the assessment of white matter tract injury and microstructural integrity, 3) proton magnetic resonance spectroscopy for quantifying proton-containing brain metabolites, 4) single photon emission computed tomography for the evaluation of nigrostriatal integrity (as assessed by presynaptic dopamine transporters and postsynaptic dopamine D2 receptors), and cerebral perfusion, 5) positron emission tomography for gauging nigrostriatal functions, glucose metabolism, amyloid and tau molecular imaging, as well as neuroinflammation, 6) myocardial scintigraphy for dysautonomia, and 7) transcranial sonography for measuring substantia nigra and lentiform nucleus echogenicity. Imaging biomarkers, using the ‘multimodal approach’, may aid in making early, accurate and objective diagnostic decisions, highlight neuroanatomical and pathophysiological mechanisms, as well as assist in evaluating disease progression and therapeutic responses to drugs in clinical trials.

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“…Imaging of striatal dopamine transporters with SPET is widely used in diagnosing the Parkinson's disease (Verhoeff 1999), since dopamine transporter density is already markedly reduced when the first symptoms appear and the results correlate well with the clinical measures of disease severity, motor impairment and asymmetry of symptomatology (Brücke et al 1997). Dopamine is a crucial neurotransmitter concerning reward and emotional responses (Wise & Rompré 1989) and, therefore, it can be assumed that dopamine neurotransmission -and possibly also dopamine transporter density -may be altered in mood and substance abuse disorders.…”

Section: Clinical Aspectsmentioning

confidence: 99%

Dopamine Transporter in vitro Binding and in vivo Imaging in the Brain

Bergström¹,

Tupala²,

Tiihonen³

2001

Pharmacology & Toxicology

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Much research interest has lately been focused on the dopamine transporter function in brain. Recent findings indicate that dopamine reuptake is more like a highly regulated than a constitutive determinant of dopamine clearance. Positron emission tomography (PET) and single-photon emission tomography (SPET) offer unique methods to study dopamine transporter function. Results from in vivo PET and SPET studies correspond well with in vitro studies performed on post mortem human brain tissue. Considering some of the variances between in vitro and in vivo receptor binding phenomena it may be that the role of a compound to alter binding to monoamine uptake sites in vitro does not indicate its potential to affect monoamine transporters after administration in vivo. This discrepancy may be better understood taking into account recent studies indicating the possibility of a rapid regulation of transporter function and surface expression. Furthermore, the dopamine transporter is a fruitful target for CNS drug discovery. Fundamental nature of drug actions in vivo may be studied using demonstrated in vitro and in vivo imaging methods.

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Measurement of the dopaminergic degeneration in Parkinson’s disease with [123I]β-CIT and SPECT

Cited by 147 publications

References 44 publications

[¹²³I]β‐CIT single‐photon emission tomography in DOPA‐responsive dystonia

[¹²³I]β‐CIT single‐photon emission tomography in DOPA‐responsive dystonia

Imaging biomarkers in Parkinson’s disease and Parkinsonian syndromes: current and emerging concepts

Dopamine Transporter in vitro Binding and in vivo Imaging in the Brain

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Measurement of the dopaminergic degeneration in Parkinson’s disease with [123I]β-CIT and SPECT

Cited by 147 publications

References 44 publications

[123I]β‐CIT single‐photon emission tomography in DOPA‐responsive dystonia

[123I]β‐CIT single‐photon emission tomography in DOPA‐responsive dystonia

Imaging biomarkers in Parkinson’s disease and Parkinsonian syndromes: current and emerging concepts

Dopamine Transporter in vitro Binding and in vivo Imaging in the Brain

Contact Info

Product

Resources

About

[¹²³I]β‐CIT single‐photon emission tomography in DOPA‐responsive dystonia

[¹²³I]β‐CIT single‐photon emission tomography in DOPA‐responsive dystonia