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Wall, Anders
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Jonasson, M., Wall, A., Chiotis, K., Leuzy, A., Eriksson, J., Antoni, G., . . . Lubberink, M. (2019). Optimal timing of tau pathology imaging and automatic extraction of a reference region using dynamic [18F]THK5317 PET.. NeuroImage: Clinical, 22, Article ID 101681.
Åpne denne publikasjonen i ny fane eller vindu >>Optimal timing of tau pathology imaging and automatic extraction of a reference region using dynamic [18F]THK5317 PET.
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2019 (engelsk)Inngår i: NeuroImage: Clinical, ISSN 0353-8842, E-ISSN 2213-1582, Vol. 22, artikkel-id 101681Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

[18F]THK5317 is a PET tracer for in-vivo imaging of tau associated with Alzheimer's disease (AD). This work aimed to evaluate optimal timing for standardized uptake value ratio (SUVR) measures with [18F]THK5317 and automated generation of SUVR-1 and relative cerebral blood flow (R1) parametric images. Nine AD patients and nine controls underwent 90 min [18F]THK5317 scans. SUVR-1 was calculated at transient equilibrium (TE) and for seven different 20 min intervals and compared with distribution volume ratio (DVR; reference Logan). Cerebellar grey matter (MRI) was used as reference region. A supervised cluster analysis (SVCA) method was implemented to automatically generate a reference region, directly from the dynamic PET volume without the need of a structural MRI scan, for computation of SUVR-1 and R1 images for a scan duration matching the optimal timing. TE was reached first in putamen, frontal- and parietal cortex at 22 ± 4 min for AD patients and in putamen at 20 ± 0 min in controls. Over all regions and subjects, SUVR20-40-1 correlated best with DVR-1, R2 = 0.97. High correlation was found between values generated using MRI- and SVCA-based reference (R2 = 0.93 for SUVR20-40-1; R2 = 0.94 for R1). SUVR20-40 allows for accurate semi-quantitative assessment of tau pathology and SVCA may be used to obtain a reference region for calculation of both SUVR-1 and R1 with 40 min scan duration.

sted, utgiver, år, opplag, sider
Elsevier, 2019
Emneord
Alzheimer's disease, PET, Parametric images, Supervised clustering, Tau imaging
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-382941 (URN)10.1016/j.nicl.2019.101681 (DOI)000470123000005 ()30710871 (PubMedID)
Forskningsfinansiär
Swedish Research Council, 05817Stockholm County CouncilGun och Bertil Stohnes StiftelseThe Karolinska Institutet's Research FoundationThe Swedish Brain FoundationSwedish Foundation for Strategic Research EU, FP7, Seventh Framework Programme
Tilgjengelig fra: 2019-05-07 Laget: 2019-05-07 Sist oppdatert: 2019-06-26bibliografisk kontrollert
Persson, J., Szalisznyo, K., Antoni, G., Wall, A., Fällmar, D., Zora, H. & Bodén, R. (2019). Phosphodiesterase 10A levels are related to striatal function in schizophrenia: a combined positron emission tomography and functional magnetic resonance imaging study. European Archives of Psychiatry and Clinical Neuroscience
Åpne denne publikasjonen i ny fane eller vindu >>Phosphodiesterase 10A levels are related to striatal function in schizophrenia: a combined positron emission tomography and functional magnetic resonance imaging study
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2019 (engelsk)Inngår i: European Archives of Psychiatry and Clinical Neuroscience, ISSN 0940-1334, E-ISSN 1433-8491Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Pharmacological inhibition of phosphodiesterase 10A (PDE10A) is being investigated as a treatment option in schizophrenia. PDE10A acts postsynaptically on striatal dopamine signaling by regulating neuronal excitability through its inhibition of cyclic adenosine monophosphate (cAMP), and we recently found it to be reduced in schizophrenia compared to controls. Here, this finding of reduced PDE10A in schizophrenia was followed up in the same sample to investigate the effect of reduced striatal PDE10A on the neural and behavioral function of striatal and downstream basal ganglia regions. A positron emission tomography (PET) scan with the PDE10A ligand [11C]Lu AE92686 was performed, followed by a 6 min resting-state magnetic resonance imaging (MRI) scan in ten patients with schizophrenia. To assess the relationship between striatal function and neurophysiological and behavioral functioning, salience processing was assessed using a mismatch negativity paradigm, an auditory event-related electroencephalographic measure, episodic memory was assessed using the Rey auditory verbal learning test (RAVLT) and executive functioning using trail-making test B. Reduced striatal PDE10A was associated with increased amplitude of low-frequency fluctuations (ALFF) within the putamen and substantia nigra, respectively. Higher ALFF in the substantia nigra, in turn, was associated with lower episodic memory performance. The findings are in line with a role for PDE10A in striatal functioning, and suggest that reduced striatal PDE10A may contribute to cognitive symptoms in schizophrenia.

HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-392015 (URN)10.1007/s00406-019-01021-0 (DOI)
Tilgjengelig fra: 2019-08-28 Laget: 2019-08-28 Sist oppdatert: 2019-08-28bibliografisk kontrollert
Altomare, D., Ferrari, C., Caroli, A., Galluzzi, S., Prestia, A., van der Flier, W. M., . . . Frisoni, G. B. (2019). Prognostic value of Alzheimer's biomarkers in mild cognitive impairment: the effect of age at onset. Journal of Neurology, 266(10), 2535-2545
Åpne denne publikasjonen i ny fane eller vindu >>Prognostic value of Alzheimer's biomarkers in mild cognitive impairment: the effect of age at onset
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2019 (engelsk)Inngår i: Journal of Neurology, ISSN 0340-5354, E-ISSN 1432-1459, Vol. 266, nr 10, s. 2535-2545Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Objective The aim of this study is to assess the impact of age at onset on the prognostic value of Alzheimer's biomarkers in a large sample of patients with mild cognitive impairment (MCI). Methods We measured A beta 42, t-tau, hippocampal volume on magnetic resonance imaging (MRI) and cortical metabolism on fluorodeoxyglucose-positron emission tomography (FDG-PET) in 188 MCI patients followed for at least 1 year. We categorised patients into earlier and later onset (EO/LO). Receiver operating characteristic curves and corresponding areas under the curve (AUCs) were performed to assess and compar the biomarker prognostic performances in EO and LO groups. Linear Model was adopted for estimating the time-to-progression in relation with earlier/later onset MCI groups and biomarkers. Results In earlier onset patients, all the assessed biomarkers were able to predict cognitive decline (p < 0.05), with FDG-PET showing the best performance. In later onset patients, all biomarkers but t-tau predicted cognitive decline (p < 0.05). Moreover, FDG-PET alone in earlier onset patients showed a higher prognostic value than the one resulting from the combination of all the biomarkers in later onset patients (earlier onset AUC 0.935 vs later onset AUC 0.753, p < 0.001). Finally, FDG-PET showed a different prognostic value between earlier and later onset patients (p = 0.040) in time-to-progression allowing an estimate of the time free from disease. Discussion FDG-PET may represent the most universal tool for the establishment of a prognosis in MCI patients and may be used for obtaining an onset-related estimate of the time free from disease.

sted, utgiver, år, opplag, sider
SPRINGER HEIDELBERG, 2019
Emneord
Alzheimer, Cognition, Imaging, Biomarkers, FDG-PET
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-395732 (URN)10.1007/s00415-019-09441-7 (DOI)000487923200022 ()31267207 (PubMedID)
Forskningsfinansiär
Swedish Research Council, 05817
Tilgjengelig fra: 2019-10-23 Laget: 2019-10-23 Sist oppdatert: 2019-10-23bibliografisk kontrollert
(2018). [15O]-H2O-PET in Premenstrual Dysphoria.
Åpne denne publikasjonen i ny fane eller vindu >>[15O]-H2O-PET in Premenstrual Dysphoria
2018 (engelsk)Annet (Annet (populærvitenskap, debatt, mm))
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-335001 (URN)
Merknad

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 March 2018).

Tilgjengelig fra: 2017-11-29 Laget: 2017-11-29 Sist oppdatert: 2018-03-16bibliografisk kontrollert
Chiotis, K., Saint-Aubert, L., Rodriguez-Vieitez, E., Leuzy, A., Almkvist, O., Savitcheva, I., . . . Nordberg, A. (2018). Longitudinal changes of tau PET imaging in relation to hypometabolism in prodromal and Alzheimer's disease dementia. Molecular Psychiatry, 23(7), 1666-1673
Åpne denne publikasjonen i ny fane eller vindu >>Longitudinal changes of tau PET imaging in relation to hypometabolism in prodromal and Alzheimer's disease dementia
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2018 (engelsk)Inngår i: Molecular Psychiatry, ISSN 1359-4184, E-ISSN 1476-5578, Vol. 23, nr 7, s. 1666-1673Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The development of tau-specific positron emission tomography (PET) tracers allows imaging in vivo the regional load of tau pathology in Alzheimer's disease (AD) and other tauopathies. Eighteen patients with baseline investigations enroled in a 17-month follow-up study, including 16 with AD (10 had mild cognitive impairment and a positive amyloid PET scan, that is, prodromal AD, and six had AD dementia) and two with corticobasal syndrome. All patients underwent PET scans with [(18)F]THK5317 (tau deposition) and [(18)F]FDG (glucose metabolism) at baseline and follow-up, neuropsychological assessment at baseline and follow-up and a scan with [(11)C]PIB (amyloid-β deposition) at baseline only. At a group level, patients with AD (prodromal or dementia) showed unchanged [(18)F]THK5317 retention over time, in contrast to significant decreases in [(18)F]FDG uptake in temporoparietal areas. The pattern of changes in [(18)F]THK5317 retention was heterogeneous across all patients, with qualitative differences both between the two AD groups (prodromal and dementia) and among individual patients. High [(18)F]THK5317 retention was significantly associated over time with low episodic memory encoding scores, while low [(18)F]FDG uptake was significantly associated over time with both low global cognition and episodic memory encoding scores. Both patients with corticobasal syndrome had a negative [(11)C]PIB scan, high [(18)F]THK5317 retention with a different regional distribution from that in AD, and a homogeneous pattern of increased [(18)F]THK5317 retention in the basal ganglia over time. These findings highlight the heterogeneous propagation of tau pathology among patients with symptomatic AD, in contrast to the homogeneous changes seen in glucose metabolism, which better tracked clinical progression.Molecular Psychiatry advance online publication, 16 May 2017; doi:10.1038/mp.2017.108.

HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-322909 (URN)10.1038/mp.2017.108 (DOI)000442358000015 ()28507319 (PubMedID)
Forskningsfinansiär
Swedish Research Council, 05817Swedish Foundation for Strategic Research Stockholm County CouncilGun och Bertil Stohnes StiftelseThe Karolinska Institutet's Research FoundationThe Swedish Brain FoundationWenner-Gren FoundationsEU, FP7, Seventh Framework ProgrammeThe Dementia Association - The National Association for the Rights of the Demented
Tilgjengelig fra: 2017-05-31 Laget: 2017-05-31 Sist oppdatert: 2018-11-05bibliografisk kontrollert
Leuzy, A., Rodriguez-Vieitez, E., Saint-Aubert, L., Chiotis, K., Almkvist, O., Savitcheva, I., . . . Nordberg, A. (2018). Longitudinal uncoupling of cerebral perfusion, glucose metabolism, and tau deposition in Alzheimer's disease.. Alzheimer's & Dementia, 14(5), 652-663
Åpne denne publikasjonen i ny fane eller vindu >>Longitudinal uncoupling of cerebral perfusion, glucose metabolism, and tau deposition in Alzheimer's disease.
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2018 (engelsk)Inngår i: Alzheimer's & Dementia, ISSN 1552-5260, E-ISSN 1552-5279, Vol. 14, nr 5, s. 652-663Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

INTRODUCTION: Cross-sectional findings using the tau tracer [18F]THK5317 (THK5317) have shown that [18F]fluorodeoxyglucose (FDG) positron emission tomography data can be approximated using perfusion measures (early-frame standardized uptake value ratio; ratio of tracer delivery in target to reference regions). In this way, a single positron emission tomography study can provide both functional and molecular information.

METHODS: We included 16 patients with Alzheimer's disease who completed follow-up THK5317 and FDG studies 17 months after baseline investigations. Linear mixed-effects models and annual percentage change maps were used to examine longitudinal change.

RESULTS: Limited spatial overlap was observed between areas showing declines in THK5317 perfusion measures and FDG. Minimal overlap was seen between areas showing functional change and those showing increased retention of THK5317.

DISCUSSION: Our findings suggest a spatiotemporal offset between functional changes and tau pathology and a partial uncoupling between perfusion and metabolism, possibly as a function of Alzheimer's disease severity.

Emneord
Alzheimer's disease, Alzheimer's disease dementia, FDG, Hypometabolism, Longitudinal study, Mild cognitive impairment, Neurofibrillary tangles, Perfusion SUVR, Perfusion imaging, Positron emission tomography (PET), Prodromal Alzheimer's disease, R(1), THK5317, Tau imaging
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-337704 (URN)10.1016/j.jalz.2017.11.008 (DOI)000432438800009 ()29268078 (PubMedID)
Forskningsfinansiär
Swedish Research Council, 05817Swedish Foundation for Strategic Research Gun och Bertil Stohnes StiftelseThe Karolinska Institutet's Research FoundationThe Swedish Brain FoundationWenner-Gren Foundations
Tilgjengelig fra: 2018-01-03 Laget: 2018-01-03 Sist oppdatert: 2018-08-01bibliografisk kontrollert
Thordardottir, S., Rodriguez-Vieitez, E., Almkvist, O., Ferreira, D., Saint-Aubert, L., Kinhult-Stahlbom, A., . . . Graff, C. (2018). Reduced penetrance of the PSEN1 H163Y autosomal dominant Alzheimer mutation: a 22-year follow-up study. Alzheimer's Research & Therapy, 10, Article ID 45.
Åpne denne publikasjonen i ny fane eller vindu >>Reduced penetrance of the PSEN1 H163Y autosomal dominant Alzheimer mutation: a 22-year follow-up study
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2018 (engelsk)Inngår i: Alzheimer's Research & Therapy, E-ISSN 1758-9193, Vol. 10, artikkel-id 45Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background: The range of onset ages within some PSEN1 families is wide, and a few cases of reduced penetrance of PSEN1 mutations have been reported. However, published data on reduced penetrance have been limited to clinical histories, often collected retrospectively and lacking biomarker information. We present a case of reduced penetrance of the PSEN1 H163Y mutation in a carrier prospectively followed for 22 years.

Methods: Two brothers (A and B), both carriers of the H163Y mutation, were followed between 1995 and 2017. They underwent repeated clinical evaluations, neuropsychological assessments, and cerebrospinal fluid analyses, as well as brain imaging examinations with structural magnetic resonance, [18F]fluorodeoxyglucose positron emission tomography, and [11C]Pittsburgh compound B positron emission tomography.

Results: Brother A was followed between 44 and 64 years of age. Cognitive symptoms due to Alzheimer’s disease set in at the age of 54. Gradual worsening of symptoms resulted in admittance to a nursing home owing to dependence on others for all activities of daily living. He showed a curvilinear decline in cognitive function on neuropsychological tests, and changes on magnetic resonance imaging, positron emission tomography, and biomarkers in the cerebrospinal fluid supported a clinical diagnosis of Alzheimer’s disease. Brother A died at the age of 64 and fulfilled the criteria for definitive Alzheimer’s disease according to neuropathological examination results. Brother B was followed between the ages of 43 and 65 and showed no cognitive deterioration on repeated neuropsychological test occasions. In addition, no biomarker evidence of Alzheimer’s disease pathology was detected, either on imaging examinations or in cerebrospinal fluid.

Conclusions: The average (SD) age of symptom onset for PSEN1 H163Y is 51 ± 7 years according to previous studies. However, we present a case of a biomarker-verified reduction in penetrance in a mutation carrier who was still symptom-free at the age of 65. This suggests that other genetic, epigenetic, and/or environmental factors modify the onset age.

Emneord
Autosomal dominant Alzheimer's disease, CSF, [F-18]fluorodeoxyglucose PET, [C-11]Pittsburgh compound B PET, Reduced penetrance
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-356491 (URN)10.1186/s13195-018-0374-y (DOI)000431827700001 ()29747683 (PubMedID)
Forskningsfinansiär
Swedish Research Council, 05817Swedish Foundation for Strategic Research Knut and Alice Wallenberg FoundationStockholm County CouncilGun och Bertil Stohnes StiftelseStiftelsen Gamla TjänarinnorÅke Wiberg Foundation
Tilgjengelig fra: 2018-07-30 Laget: 2018-07-30 Sist oppdatert: 2019-05-09bibliografisk kontrollert
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
Åpne denne publikasjonen i ny fane eller vindu >>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 (engelsk)Inngår i: Journal of Alzheimer's Disease, ISSN 1387-2877, E-ISSN 1875-8908, Vol. 59, nr 2, s. 603-614Artikkel i tidsskrift (Fagfellevurdert) 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.

Emneord
Alzheimer's disease, C-11-PiB-PET, conversion prediction, dementia, early diagnosis, F-18-FDG-PET, mild cognitive impairment, prognosis
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-331961 (URN)10.3233/JAD-170158 (DOI)000405805400019 ()
Forskningsfinansiär
EU, FP7, Seventh Framework Programme, 278850, HEALTH-F2-2011278850Swedish Research Council, 05817Swedish Foundation for Strategic Research The Swedish Brain FoundationWenner-Gren Foundations
Tilgjengelig fra: 2017-10-20 Laget: 2017-10-20 Sist oppdatert: 2017-10-20bibliografisk kontrollert
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
Åpne denne publikasjonen i ny fane eller vindu >>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 (engelsk)Inngår i: Journal of Cerebral Blood Flow and Metabolism, ISSN 0271-678X, E-ISSN 1559-7016, Vol. 37, nr 2, s. 740-749Artikkel i tidsskrift (Fagfellevurdert) 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.

sted, utgiver, år, opplag, sider
SAGE PUBLICATIONS INC, 2017
Emneord
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
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-319114 (URN)10.1177/0271678X16645593 (DOI)000393903900029 ()27107028 (PubMedID)
Forskningsfinansiär
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
Tilgjengelig fra: 2017-04-03 Laget: 2017-04-03 Sist oppdatert: 2017-11-29bibliografisk kontrollert
Vedung, F., Antoni, G., Wall, A., Fahlström, M., Larsson, E.-M. & Marklund, N. (2017). Persistent Decrease Of Cerebral Blood Flow In Traumatic Brain Injury And Sports-Related Concussion. Paper presented at 35th Annual National Neurotrauma Symposium, JUL 07-12, 2017, Snowbird, UT. Journal of Neurotrauma, 34(13), A8-A9
Åpne denne publikasjonen i ny fane eller vindu >>Persistent Decrease Of Cerebral Blood Flow In Traumatic Brain Injury And Sports-Related Concussion
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2017 (engelsk)Inngår i: Journal of Neurotrauma, ISSN 0897-7151, E-ISSN 1557-9042, Vol. 34, nr 13, s. A8-A9Artikkel i tidsskrift, Meeting abstract (Annet vitenskapelig) Published
Emneord
Cerebral perfusion, Concussion, ASL, athletes
HSV kategori
Identifikatorer
urn:nbn:se:uu:diva-335815 (URN)10.1089/neu.2017.29011.abstracts (DOI)000404530400021 ()
Konferanse
35th Annual National Neurotrauma Symposium, JUL 07-12, 2017, Snowbird, UT
Forskningsfinansiär
Swedish Research CouncilThe Swedish Brain Foundation
Tilgjengelig fra: 2018-01-22 Laget: 2018-01-22 Sist oppdatert: 2018-01-22bibliografisk kontrollert
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