MR relaxometry and 1H MR spectroscopy for the determination of iron and metabolite concentrations in PKAN patients

Hájek, Milan; Adamovičová, Miriam; Herynek, Vı́t; Škoch, Antonín; Jírů, Filip; Křepelová, Anna; Dezortová, Monika

doi:10.1007/s00330-004-2553-4

Cited by 27 publications

(29 citation statements)

References 29 publications

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“…Due to the limited resolution of the SI data and the omission of the correction for CSF content in each voxel, the concentration values are subject to partial volume effects. The metabolite image shows an increased concentration of Cr in the basal ganglia, which is in accordance with the published data[21,22]. On the other hand, the image shows very low Cr concentrations in the middle frontal region.…”

supporting

confidence: 90%

Error images for spectroscopic imaging by LCModel using Cramer–Rao bounds

Jírů

Škoch

Klose

et al. 2006

Magn Reson Mater Phy

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The results of spectroscopic imaging (SI) measurements are often presented as metabolic images. If the spectra quality is not sufficient, the calculated concentrations are biased and the metabolic images show an incorrect metabolite distribution. To simplify the quality analysis of spectra measured by SI, an error image, reflecting the accuracy of the computed concentrations, can be displayed along with the metabolite image. In this paper the relevance of Cramer-Rao bounds (CRBs) calculated by the LCModel program to describe errors in estimated concentrations is validated using spectra simulations. The relation between the average CRBs and standard deviations (STD) of metabolite concentrations from 100 simulated spectra for various signal to noise ratio and line broadening conditions is evaluated. A parameter for calculating error images for metabolite ratios is proposed and an effective way to display error images is shown. The results suggest that the average CRBs are strongly correlated with the standard deviations and hence that CRB values reflect the relative uncertainty of the calculated concentrations. The error information can be integrated directly into a metabolite image by displaying only those areas of the metabolite image with corresponding CRBs below a selected threshold or by mapping CRBs as a transparency of the metabolite image. The concept of error images avoids extensive examination of each SI spectrum and helps to reject low quality spectra.

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supporting

confidence: 90%

Error images for spectroscopic imaging by LCModel using Cramer–Rao bounds

Jírů

Škoch

Klose

et al. 2006

Magn Reson Mater Phy

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“…jpet.aspetjournals.org levels are high in vulnerable brain regions and are increased further in these diseases (Zecca et al, 2004). The iron concentration that we used is similar to that used in other in vitro studies of iron neurotoxicity (Liu et al, 2003) and within the range of concentrations found in mouse and human brain (Griffiths et al, 1999;Moos et al, 2000;Zecca et al, 2001;Hajek et al, 2004).…”

Section: Discussionmentioning

confidence: 98%

Involvement of Protein Kinase A in Cannabinoid Receptor-Mediated Protection from Oxidative Neuronal Injury

Kim¹,

Won²,

Mao³

et al. 2004

J Pharmacol Exp Ther

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CB1 cannabinoid receptors (CB1Rs) are involved in protecting the brain from ischemia and related disorders. However, the underlying protective mechanisms are incompletely understood. We investigated the effect of CB1R activation on oxidative injury, which has been implicated in neuronal death after cerebral ischemia and neurodegenerative disorders, in mouse cortical neuron cultures.methanone mesylate] reduced neuronal death, measured by lactate dehydrogenase release, in cultures treated with 50 M FeCl 2 , and its protective effect was attenuated by the CB1R antagonist SR141716A [N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-cichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide hydrochloride]. The endocannabinoid anandamide reproduced the effect of Win 55212-2, as did the antioxidant 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid (Trolox). Neuronal injury was more severe after in vitro or in vivo administration of FeCl 2 to CB1R-knockout compared with wild-type mice. Win 55212-2 reduced the formation of reactive oxidative species in cortical neuron cultures treated with FeCl 2 , consistent with an antioxidant action. Pertussis toxin reduced CB1R-mediated protection, which points to a protective mechanism that involves signaling through G i/o proteins. Since CB1R-activated G protein signaling inhibits protein kinase A but activates phosphatidylinositol 3-kinase (PI3K), we tested the involvement of these pathways in CB1R-mediated neuroprotection. Dibutyryl-cyclic adenosine monophosphate (dbcAMP) blocked protection by Win 55212-2, whereas the PI3K inhibitor wortmannin did not, and the effect of dbcAMP was inhibited by the protein kinase A inhibitor H89 [N-[2-((p-bromocinnamyl)amino)ethyl]-5-isoquinolinesulfonamide] (Ն10 nM). CB1R-induced, SR141716A-, pertussis toxin-, and dbcAMP-sensitive protection was also observed for two other oxidative insults, exposure to H 2 O 2 or buthionine sulfoximine. Therefore, receptor-stimulated inhibition of protein kinase A seems to be required for the neuroprotective effect of CB1R activation against oxidative neuronal injury.Endogenous cannabinoid (endocannabinoid) signaling pathways, consisting of endocannabinoids such as anandamide and 2-arachidonylglycerol and the G protein-coupled CB1R and CB2R receptors, have been implicated in a range of physiological brain functions. In addition, endocannabinoid signaling provides neuroprotection after ischemia and other cerebral insults. Cannabinoid receptor agonists reduce neuronal loss from global and focal cerebral ischemia (Nagayama et al., 1999) and brain trauma (Panikashvili et al., 2001), and the size of cerebral infarcts after middle cerebral artery occlusion is increased in CB1R-knockout mice (ParmentierBatteur et al., 2002). The brain's response to ischemia involves up-regulation of neuronal CB1 receptors (Jin et al., 2000) and increased production of endocannabinoid-related compounds that modulate the inflammatory response to ischemia (Franklin et al., 2003). Therefore, endogenous cannabinoid signaling mechanisms may...

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“…5). As these results had been theoretically forecasted based on published experimental studies [23,24], no correction for multiple comparisons was employed in the statistical analysis of these data. The correlation for the right pallidum and caudate were slightly less than statistically significant.…”

Section: Correlation Between Relaxometry Clinical and Genetic Paramementioning

confidence: 99%

MR relaxometry in Huntington's disease: Correlation between imaging, genetic and clinical parameters

Vymazal

Klempíř

Jech

et al. 2007

Journal of the Neurological Sciences

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MR relaxometry and 1H MR spectroscopy for the determination of iron and metabolite concentrations in PKAN patients

Cited by 27 publications

References 29 publications

Error images for spectroscopic imaging by LCModel using Cramer–Rao bounds

Error images for spectroscopic imaging by LCModel using Cramer–Rao bounds

Involvement of Protein Kinase A in Cannabinoid Receptor-Mediated Protection from Oxidative Neuronal Injury

MR relaxometry in Huntington's disease: Correlation between imaging, genetic and clinical parameters

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