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Wall, Anders
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Publications (10 of 49) Show all publications
(2017). [15O]-H2O-PET in Premenstrual Dysphoria. .
Open this publication in new window or tab >>[15O]-H2O-PET in Premenstrual Dysphoria
2017 (English)Other (Other (popular science, discussion, etc.))
National Category
Obstetrics, Gynecology and Reproductive Medicine
Identifiers
urn:nbn:se:uu:diva-335001 (URN)
Note

Dataset till en artikel:

Eriksson, O, Wall, A, Olsson, U, Marteinsdottir, I, Holstad, M, Ågren, H, Hartvig, P, Långström, B, Naessén, T. "Women with Premenstrual Dysphoria show signs of an Asymmetric Frontal Brain Activity with R > L in both Phases of the Menstrual Cycle" (submitted December 2017).

Available from: 2017-11-29 Created: 2017-11-29 Last updated: 2017-11-29Bibliographically approved
Iaccarino, L., Chiotis, K., Alongi, P., Almkvist, O., Wall, A., Cerami, C., . . . Perani, D. (2017). A Cross-Validation of FDG- and Amyloid-PET Biomarkers in Mild Cognitive Impairment for the Risk Prediction to Dementia due to Alzheimer's Disease in a Clinical Setting. Journal of Alzheimer's Disease, 59(2), 603-614.
Open this publication in new window or tab >>A Cross-Validation of FDG- and Amyloid-PET Biomarkers in Mild Cognitive Impairment for the Risk Prediction to Dementia due to Alzheimer's Disease in a Clinical Setting
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2017 (English)In: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 59, no 2, 603-614 p.Article in journal (Refereed) Published
Abstract [en]

Assessments of brain glucose metabolism (F-18-FDG-PET) and cerebral amyloid burden (C-11-PiB-PET) in mild cognitive impairment (MCI) have shown highly variable performances when adopted to predict progression to dementia due to Alzheimer's disease (ADD). This study investigates, in a clinical setting, the separate and combined values of F-18-FDGPET and C-11-PiB-PET in ADD conversion prediction with optimized data analysis procedures. Respectively, we investigate the accuracy of an optimized SPM analysis for F-18-FDG-PET and of standardized uptake value ratio semiquantification for C-11-PiB-PET in predicting ADD conversion in 30 MCI subjects (age 63.57 +/- 7.78 years). Fourteen subjects converted to ADD during the follow-up (median 26.5 months, inter-quartile range 30 months). Receiver operating characteristic analyses showed an area under the curve (AUC) of 0.89 and of 0.81 for, respectively, F-18-FDG-PET and C-11-PiB-PET. F-18-FDG-PET, compared to C-11-PiB-PET, showed higher specificity (1.00 versus 0.62, respectively), but lower sensitivity (0.79 versus 1.00). Combining the biomarkers improved classification accuracy (AUC = 0.96). During the follow-up time, all the MCI subjects positive for both PET biomarkers converted to ADD, whereas all the subjects negative for both remained stable. The difference in survival distributions was confirmed by a log-rank test (p = 0.002). These results indicate a very high accuracy in predicting MCI to ADD conversion of both F-18-FDG-PET and C-11-PiB-PET imaging, the former showing optimal performance based on the SPM optimized parametric assessment. Measures of brain glucose metabolism and amyloid load represent extremely powerful diagnostic and prognostic biomarkers with complementary roles in prodromal dementia phase, particularly when tailored to individual cases in clinical settings.

Keyword
Alzheimer's disease, C-11-PiB-PET, conversion prediction, dementia, early diagnosis, F-18-FDG-PET, mild cognitive impairment, prognosis
National Category
Neurology Radiology, Nuclear Medicine and Medical Imaging
Identifiers
urn:nbn:se:uu:diva-331961 (URN)10.3233/JAD-170158 (DOI)000405805400019 ()
Funder
EU, FP7, Seventh Framework Programme, 278850, HEALTH-F2-2011278850Swedish Research Council, 05817Swedish Foundation for Strategic Research The Swedish Brain FoundationWenner-Gren Foundations
Available from: 2017-10-20 Created: 2017-10-20 Last updated: 2017-10-20Bibliographically approved
Rodriguez-Vieitez, E., Leuzy, A., Chiotis, K., Saint-Aubert, L., Wall, A. & Nordberg, A. (2017). Comparability of [F-18]THK5317 and [C-11]PIB blood flow proxy images with [F-18]FDG positron emission tomography in Alzheimer's disease. Journal of Cerebral Blood Flow and Metabolism, 37(2), 740-749.
Open this publication in new window or tab >>Comparability of [F-18]THK5317 and [C-11]PIB blood flow proxy images with [F-18]FDG positron emission tomography in Alzheimer's disease
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2017 (English)In: Journal of Cerebral Blood Flow and Metabolism, ISSN 0271-678X, E-ISSN 1559-7016, Vol. 37, no 2, 740-749 p.Article in journal (Refereed) Published
Abstract [en]

For amyloid positron emission tomography tracers, the simplified reference tissue model derived ratio of influx rate in target relative to reference region (R-1) has been shown to serve as a marker of brain perfusion, and, due to the strong coupling between perfusion and metabolism, as a proxy for glucose metabolism. In the present study, 11 prodromal Alzheimer's disease and nine Alzheimer's disease dementia patients underwent [F-18]THK5317, carbon-11 Pittsburgh Compound-B ([C-11]PIB), and 2-deoxy-2-[F-18]fluoro-D-glucose ([F-18]FDG) positron emission tomography to assess the possible use of early-phase [F-18]THK5317 and R-1 as proxies for brain perfusion, and thus, for glucose metabolism. Discriminative performance (prodromal vs Alzheimer's disease dementia) of [F-18]THK5317 (early-phase SUVr and R-1) was compared with that of [C-11]PIB (early-phase SUVr and R-1) and [F-18]FDG. Strong positive correlations were found between [F-18]THK5317 (early-phase, R-1) and [F-18]FDG, particularly in frontal and temporoparietal regions. Differences in correlations between early-phase and R-1 ([F-18]THK5317 and [C-11]PIB) and [F-18]FDG, were not statistically significant, nor were differences in area under the curve values in the discriminative analysis. Our findings suggest that early-phase [F-18]THK5317 and R-1 provide information on brain perfusion, closely related to glucose metabolism. As such, a single positron emission tomography study with [F-18]THK5317 may provide information about both tau pathology and brain perfusion in Alzheimer's disease, with potential clinical applications.

Place, publisher, year, edition, pages
SAGE PUBLICATIONS INC, 2017
Keyword
Alzheimer's disease, early-phase carbon-11 Pittsburgh Compound-B, early-phase [F-18]THK5317 positron emission tomography, 2-deoxy-2-[F-18]fluoro-D-glucose, simplified reference tissue model R-1
National Category
Endocrinology and Diabetes Hematology Neurology
Identifiers
urn:nbn:se:uu:diva-319114 (URN)10.1177/0271678X16645593 (DOI)000393903900029 ()27107028 (PubMedID)
Funder
Swedish Research Council, 05817Swedish Foundation for Strategic Research The Karolinska Institutet's Research FoundationThe Swedish Brain FoundationThe Dementia Association - The National Association for the Rights of the DementedEU, European Research Council, HEALTH-F2-2011-278850Stiftelsen Gamla TjänarinnorWenner-Gren Foundations
Available from: 2017-04-03 Created: 2017-04-03 Last updated: 2017-11-29Bibliographically approved
Bodén, R., Persson, J., Wall, A., Lubberink, M., Ekselius, L., Larsson, E.-M. & Antoni, G. (2017). Striatal Phosphodiesterase 10A and Medial Prefrontal Cortical Thickness in Patients with Schizophrenia: A PET and MRI Study. Paper presented at 72nd Annual Scientific Convention and Meeting of the Society-of-Biological-Psychiatry (SOBP), MAY 18-20, 2017, San Diego, CA. Biological Psychiatry, 81(10), S386-S387.
Open this publication in new window or tab >>Striatal Phosphodiesterase 10A and Medial Prefrontal Cortical Thickness in Patients with Schizophrenia: A PET and MRI Study
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2017 (English)In: Biological Psychiatry, ISSN 0006-3223, E-ISSN 1873-2402, Vol. 81, no 10, S386-S387 p.Article in journal, Meeting abstract (Other academic) Published
Keyword
Schizophrenia, Positron Emission Tomography, Magnetic resonance imaging, striatum, Cortical Thickness
National Category
Psychiatry Radiology, Nuclear Medicine and Medical Imaging
Identifiers
urn:nbn:se:uu:diva-331804 (URN)10.1016/j.biopsych.2017.02.681 (DOI)000400348701048 ()
Conference
72nd Annual Scientific Convention and Meeting of the Society-of-Biological-Psychiatry (SOBP), MAY 18-20, 2017, San Diego, CA
Available from: 2017-10-18 Created: 2017-10-18 Last updated: 2017-10-18Bibliographically approved
Bodén, R., Persson, J., Wall, A., Lubberink, M., Ekselius, L., Larsson, E.-M. & Antoni, G. (2017). Striatal phosphodiesterase 10A and medial prefrontal cortical thickness in patients with schizophrenia: a PET and MRI study. Translational Psychiatry, 7(3), Article ID e1050.
Open this publication in new window or tab >>Striatal phosphodiesterase 10A and medial prefrontal cortical thickness in patients with schizophrenia: a PET and MRI study
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2017 (English)In: Translational Psychiatry, ISSN 2158-3188, E-ISSN 2158-3188, Vol. 7, no 3, e1050Article in journal (Refereed) Published
Abstract [en]

The enzyme phosphodiesterase 10A (PDE10A) is abundant in striatal medium spiny neurons and has been implicated in the pathophysiology of schizophrenia in animal models and is investigated as a possible new pharmacological treatment target. A reduction of prefrontal cortical thickness is common in schizophrenia, but how this relates to PDE10A expression is unknown. Our study aim was to compare, we believe for the first time, the striatal non-displaceable binding potential (BPND) of the new validated PDE10A ligand [(11)C]Lu AE92686 between patients with schizophrenia and healthy controls. Furthermore, we aimed to assess the correlation of PDE10A BPND to cortical thickness. Sixteen healthy male controls and 10 male patients with schizophrenia treated with clozapine, olanzapine or quetiapine were investigated with positron emission tomography (PET) and magnetic resonance imaging (MRI). Striatal binding potential (BPND) of [(11)C]Lu AE92686 was acquired through dynamic PET scans and cortical thickness by structural MRI. Clinical assessments of symptoms and cognitive function were performed and the antipsychotic dosage was recorded. Patients with schizophrenia had a significantly lower BPND of [(11)C]Lu AE92686 in striatum (P=0.003) than healthy controls. The striatal BPND significantly correlated to cortical thickness in the medial prefrontal cortex and superior frontal gyrus across patients with schizophrenia and healthy controls. No significant correlation was observed between the BPND for [(11)C]Lu AE92686 in striatum and age, schizophrenia symptoms, antipsychotic dosage, coffee consumption, smoking, duration of illness or cognitive function in the patients. In conclusion, PDE10A may be important for functioning in the striato-cortical interaction and in the pathophysiology of schizophrenia.

National Category
Psychiatry Medicinal Chemistry
Identifiers
urn:nbn:se:uu:diva-316901 (URN)10.1038/tp.2017.11 (DOI)000397228200002 ()28267149 (PubMedID)
Funder
Swedish Research Council, 2016-02362
Available from: 2017-03-08 Created: 2017-03-08 Last updated: 2018-01-13Bibliographically approved
Rodriguez-Vieitez, E., Carter, S. F., Chiotis, K., Saint-Aubert, L., Leuzy, A., Scholl, M., . . . Nordberg, A. (2016). Comparison of Early-Phase C-11-Deuterium-L-Deprenyl and C-11-Pittsburgh Compound B PET for Assessing Brain Perfusion in Alzheimer Disease. Journal of Nuclear Medicine, 57(7), 1071-1077.
Open this publication in new window or tab >>Comparison of Early-Phase C-11-Deuterium-L-Deprenyl and C-11-Pittsburgh Compound B PET for Assessing Brain Perfusion in Alzheimer Disease
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2016 (English)In: Journal of Nuclear Medicine, ISSN 0161-5505, E-ISSN 1535-5667, Vol. 57, no 7, 1071-1077 p.Article in journal (Refereed) Published
Abstract [en]

The PET tracer C-11-deuterium-L-deprenyl (C-11-DED) has been used to visualize activated astrocytes in vivo in patients with Alzheimer disease (AD). In this multitracer PET study, early-phase C-11-DED and C-11-Pittsburgh compound B (C-11-PiB) (eDED and ePiB, respectively) were compared as surrogate markers of brain perfusion, and the extent to which C-11-DED binding is influenced by brain perfusion was investigated. METHODS: C-11-DED, C-11-PiB, and F-18-FDG dynamic PET scans were obtained in age-matched groups comprising AD patients (n = 8), patients with mild cognitive impairment (n = 17), and healthy controls (n = 16). A modified reference Patlak model was used to quantify C-11-DED binding. A simplified reference tissue model was applied to both C-11-DED and C-11-PiB to measure brain perfusion relative to the cerebellar gray matter (R-1) and binding potentials. C-11-PiB retention and F-18-FDG uptake were also quantified as target-to-pons SUV ratios in 12 regions of interest (ROIs). RESULTS: The strongest within-subject correlations with the corresponding R-1 values (R-1,R-DED and R-1,R-PiB, respectively) and with F-18-FDG uptake were obtained when the eDED and ePiB PET data were measured 1-4 min after injection. The optimum eDED/ePiB intervals also showed strong, significant ROI-based intersubject Pearson correlations with R-1,R-DED/R-1,R-PiB and with F-18-FDG uptake, whereas C-11-DED binding was largely independent of brain perfusion, as measured by eDED. Corresponding voxelwise correlations confirmed the ROI-based results. Temporoparietal eDED or ePiB brain perfusion measurements were highly discriminative between patient and control groups, with discriminative ability statistically comparable to that of temporoparietal F-18-FDG glucose metabolism. Hypometabolism extended over wider regions than hypoperfusion in patient groups compared with controls. CONCLUSION: The 1- to 4-min early-frame intervals of C-11-DED or C-11-PiB are suitable surrogate measures for brain perfusion. C-11-DED binding is independent of brain perfusion, and thus C-11-DED PET can provide information on both functional (brain perfusion) and pathologic (astrocytosis) aspects from a single PET scan. In comparison with glucose metabolism, early-phase C-11-DED and C-11-PiB perfusion appear to provide complementary rather than redundant information.

Keyword
amyloid, astrocytosis, brain perfusion, early-phase PET
National Category
Radiology, Nuclear Medicine and Medical Imaging
Identifiers
urn:nbn:se:uu:diva-300056 (URN)10.2967/jnumed.115.168732 (DOI)000378979200016 ()26912447 (PubMedID)
Funder
Swedish Research Council, 05817Swedish Foundation for Strategic Research Knut and Alice Wallenberg FoundationThe Karolinska Institutet's Research FoundationThe Swedish Brain FoundationThe Dementia Association - The National Association for the Rights of the DementedEU, FP7, Seventh Framework ProgrammeStiftelsen Gamla TjänarinnorWenner-Gren Foundations
Available from: 2016-08-02 Created: 2016-08-02 Last updated: 2017-11-28Bibliographically approved
Rodriguez-Vieitez, E., Saint-Aubert, L., Carter, S. F., Almkvist, O., Farid, K., Scholl, M., . . . Nordberg, A. (2016). Diverging longitudinal changes in astrocytosis and amyloid PET in autosomal dominant Alzheimer's disease. Brain, 139(3), 922-936.
Open this publication in new window or tab >>Diverging longitudinal changes in astrocytosis and amyloid PET in autosomal dominant Alzheimer's disease
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2016 (English)In: Brain, ISSN 0006-8950, E-ISSN 1460-2156, Vol. 139, no 3, 922-936 p.Article in journal (Refereed) Published
Abstract [en]

The relationships between pathophysiological processes in Alzheimer's disease remain largely unclear. In a longitudinal, multitracer PET study, Rodriguez-Vieitez et al. reveal that progression of autosomal dominant Alzheimer's disease is accompanied by prominent early and then declining astrocytosis, increasing amyloid plaque deposition and decreasing glucose metabolism. Astrocyte activation may initiate Alzheimer pathology.See Schott and Fox (doi: 10.1093/brain/awv405) for a scientific commentary on this article. The relationships between pathophysiological processes in Alzheimer's disease remain largely unclear. In a longitudinal, multitracer PET study, Rodriguez-Vieitez et al. reveal that progression of autosomal dominant Alzheimer's disease is accompanied by prominent early and then declining astrocytosis, increasing amyloid plaque deposition and decreasing glucose metabolism. Astrocyte activation may initiate Alzheimer pathology.Alzheimer's disease is a multifactorial dementia disorder characterized by early amyloid-beta, tau deposition, glial activation and neurodegeneration, where the interrelationships between the different pathophysiological events are not yet well characterized. In this study, longitudinal multitracer positron emission tomography imaging of individuals with autosomal dominant or sporadic Alzheimer's disease was used to quantify the changes in regional distribution of brain astrocytosis (tracer C-11-deuterium-L-deprenyl), fibrillar amyloid-beta plaque deposition (C-11-Pittsburgh compound B), and glucose metabolism (F-18-fluorodeoxyglucose) from early presymptomatic stages over an extended period to clinical symptoms. The 52 baseline participants comprised autosomal dominant Alzheimer's disease mutation carriers (n = 11; 49.6 +/- 10.3 years old) and non-carriers (n = 16; 51.1 +/- 14.2 years old; 10 male), and patients with sporadic mild cognitive impairment (n = 17; 61.9 +/- 6.4 years old; nine male) and sporadic Alzheimer's disease (n = 8; 63.0 +/- 6.5 years old; five male); for confidentiality reasons, the gender of mutation carriers is not revealed. The autosomal dominant Alzheimer's disease participants belonged to families with known mutations in either presenilin 1 (PSEN1) or amyloid precursor protein (APPswe or APParc) genes. Sporadic mild cognitive impairment patients were further divided into C-11-Pittsburgh compound B-positive (n = 13; 62.0 +/- 6.4; seven male) and C-11-Pittsburgh compound B-negative (n = 4; 61.8 +/- 7.5 years old; two male) groups using a neocortical standardized uptake value ratio cut-off value of 1.41, which was calculated with respect to the cerebellar grey matter. All baseline participants underwent multitracer positron emission tomography scans, cerebrospinal fluid biomarker analysis and neuropsychological assessment. Twenty-six of the participants underwent clinical and imaging follow-up examinations after 2.8 +/- 0.6 years. By using linear mixed-effects models, fibrillar amyloid-beta plaque deposition was first observed in the striatum of presymptomatic autosomal dominant Alzheimer's disease carriers from 17 years before expected symptom onset; at about the same time, astrocytosis was significantly elevated and then steadily declined. Diverging from the astrocytosis pattern, amyloid-beta plaque deposition increased with disease progression. Glucose metabolism steadily declined from 10 years after initial amyloid-beta plaque deposition. Patients with sporadic mild cognitive impairment who were C-11-Pittsburgh compound B-positive at baseline showed increasing amyloid-beta plaque deposition and decreasing glucose metabolism but, in contrast to autosomal dominant Alzheimer's disease carriers, there was no significant longitudinal decline in astrocytosis over time. The prominent initially high and then declining astrocytosis in autosomal dominant Alzheimer's disease carriers, contrasting with the increasing amyloid-beta plaque load during disease progression, suggests astrocyte activation is implicated in the early stages of Alzheimer's disease pathology.

Keyword
astrocytosis, autosomal dominant Alzheimer's disease, C-11-deuterium-L-deprenyl, F-18-fluorodeoxyglucose, C-11-Pittsburgh compound B
National Category
Neurology
Identifiers
urn:nbn:se:uu:diva-282820 (URN)10.1093/brain/awv404 (DOI)000371694600031 ()26813969 (PubMedID)
Funder
Swedish Research Council, 05817Swedish Foundation for Strategic Research Knut and Alice Wallenberg FoundationStockholm County CouncilThe Swedish Brain FoundationThe Dementia Association - The National Association for the Rights of the DementedEU, European Research CouncilStiftelsen Gamla TjänarinnorWenner-Gren Foundations
Available from: 2016-04-07 Created: 2016-04-07 Last updated: 2017-11-30Bibliographically approved
Chiotis, K., Saint-Aubert, L., Savitcheva, I., Jelic, V., Andersen, P., Jonasson, M., . . . Nordberg, A. (2016). Imaging in-vivo tau pathology in Alzheimer's disease with THK5317 PET in a multimodal paradigm. European Journal of Nuclear Medicine and Molecular Imaging, 43(9), 1686-1699.
Open this publication in new window or tab >>Imaging in-vivo tau pathology in Alzheimer's disease with THK5317 PET in a multimodal paradigm
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2016 (English)In: European Journal of Nuclear Medicine and Molecular Imaging, ISSN 1619-7070, E-ISSN 1619-7089, Vol. 43, no 9, 1686-1699 p.Article in journal (Refereed) Published
Abstract [en]

PURPOSE: The aim of this study was to explore the cerebral distribution of the tau-specific PET tracer [(18)F]THK5317 (also known as (S)-[(18)F]THK5117) retention in different stages of Alzheimer's disease; and study any associations with markers of hypometabolism and amyloid-beta deposition.

METHODS: Thirty-three individuals were enrolled, including nine patients with Alzheimer's disease dementia, thirteen with mild cognitive impairment (MCI), two with non-Alzheimer's disease dementia, and nine healthy controls (five young and four elderly). In a multi-tracer PET design [(18)F]THK5317, [(11)C] Pittsburgh compound B ([(11)C]PIB), and [(18)F]FDG were used to assess tau pathology, amyloid-beta deposition and cerebral glucose metabolism, respectively. The MCI patients were further divided into MCI [(11)C]PIB-positive (n = 11) and MCI [(11)C]PIB-negative (n = 2) groups.

RESULTS: Test-retest variability for [(18)F]THK5317-PET was very low (1.17-3.81 %), as shown by retesting five patients. The patients with prodromal (MCI [(11)C]PIB-positive) and dementia-stage Alzheimer's disease had significantly higher [(18)F]THK5317 retention than healthy controls (p = 0.002 and p = 0.001, respectively) in areas exceeding limbic regions, and their discrimination from this control group (using the area under the curve) was >98 %. Focal negative correlations between [(18)F]THK5317 retention and [(18)F]FDG uptake were observed mainly in the frontal cortex, and focal positive correlations were found between [(18)F]THK5317 and [(11)C]PIB retentions isocortically. One patient with corticobasal degeneration syndrome and one with progressive supranuclear palsy showed no [(11)C]PIB but high [(18)F]THK5317 retentions with a different regional distribution from that in Alzheimer's disease patients.

CONCLUSIONS: The tau-specific PET tracer [(18)F]THK5317 images in vivo the expected regional distribution of tau pathology. This distribution contrasts with the different patterns of hypometabolism and amyloid-beta deposition.

National Category
Radiology, Nuclear Medicine and Medical Imaging
Identifiers
urn:nbn:se:uu:diva-281916 (URN)10.1007/s00259-016-3363-z (DOI)000379017500015 ()26996778 (PubMedID)
External cooperation:
Funder
Swedish Research Council, 05817The Karolinska Institutet's Research FoundationStiftelsen Gamla TjänarinnorThe Swedish Brain FoundationThe Dementia Association - The National Association for the Rights of the DementedWenner-Gren FoundationsEU, European Research Council, HEALTH-F2-2011-278850Swedish Foundation for Strategic Research
Available from: 2016-03-31 Created: 2016-03-31 Last updated: 2017-11-30Bibliographically approved
Bodén, R., Persson, J., Wall, A., Lubberink, M., Ekselius, L., Larsson, E. & Antoni, G. (2016). Striatal Phosphodiesterase 10A and Thinning of the medial Prefrontal Cortex in Schizophrenia - a PET and MRI study. Paper presented at Annual Congress of the European-Association-of-Nuclear-Medicine (EANM), OCT 15-19, 2016, Barcelona, SPAIN. European Journal of Nuclear Medicine and Molecular Imaging, 43, S48-S49.
Open this publication in new window or tab >>Striatal Phosphodiesterase 10A and Thinning of the medial Prefrontal Cortex in Schizophrenia - a PET and MRI study
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2016 (English)In: European Journal of Nuclear Medicine and Molecular Imaging, ISSN 1619-7070, E-ISSN 1619-7089, Vol. 43, S48-S49 p.Article in journal, Meeting abstract (Refereed) Published
National Category
Radiology, Nuclear Medicine and Medical Imaging
Identifiers
urn:nbn:se:uu:diva-316215 (URN)000391801600102 ()
Conference
Annual Congress of the European-Association-of-Nuclear-Medicine (EANM), OCT 15-19, 2016, Barcelona, SPAIN
Available from: 2017-02-27 Created: 2017-02-27 Last updated: 2017-11-29Bibliographically approved
Jonasson, M., Wall, A., Chiotis, K., Heurling, K., Saint-Aubert, L., Antoni, G., . . . Lubberink, M. (2016). Supervised Cluster Analysis for Automatic Extraction of Reference Region in Dynamic [F-18]THK5317 PET. Paper presented at Annual Congress of the European-Association-of-Nuclear-Medicine (EANM), OCT 15-19, 2016, Barcelona, SPAIN. European Journal of Nuclear Medicine and Molecular Imaging, 43, S25-S25.
Open this publication in new window or tab >>Supervised Cluster Analysis for Automatic Extraction of Reference Region in Dynamic [F-18]THK5317 PET
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2016 (English)In: European Journal of Nuclear Medicine and Molecular Imaging, ISSN 1619-7070, E-ISSN 1619-7089, Vol. 43, S25-S25 p.Article in journal, Meeting abstract (Refereed) Published
National Category
Radiology, Nuclear Medicine and Medical Imaging
Identifiers
urn:nbn:se:uu:diva-316219 (URN)000391801600039 ()
Conference
Annual Congress of the European-Association-of-Nuclear-Medicine (EANM), OCT 15-19, 2016, Barcelona, SPAIN
Available from: 2017-02-27 Created: 2017-02-27 Last updated: 2017-11-29Bibliographically approved
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