000902565 001__ 902565
000902565 005__ 20250414120445.0
000902565 0247_ $$2doi$$a10.1093/braincomms/fcab306
000902565 0247_ $$2Handle$$a2128/30729
000902565 0247_ $$2altmetric$$aaltmetric:121159480
000902565 0247_ $$2pmid$$a35291442
000902565 0247_ $$2WOS$$aWOS:000804710200027
000902565 037__ $$aFZJ-2021-04364
000902565 082__ $$a610
000902565 1001_ $$0P:(DE-HGF)0$$aDeistung, A.$$b0$$eCorresponding author
000902565 245__ $$aQuantitative suspecptibility mapping reveals alterations of denate nuclei in common types of ataxias
000902565 260__ $$a[Großbritannien]$$bGuarantors of Brain$$c2022
000902565 3367_ $$2DRIVER$$aarticle
000902565 3367_ $$2DataCite$$aOutput Types/Journal article
000902565 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1645106745_22170
000902565 3367_ $$2BibTeX$$aARTICLE
000902565 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000902565 3367_ $$00$$2EndNote$$aJournal Article
000902565 520__ $$aThe cerebellar nuclei are a brain region with high iron content. Surprisingly, little is known about iron content in the cerebellar nuclei and its possible contribution to pathology in cerebellar ataxias, with the only exception of Friedreich’s ataxia. In the present exploratory cross-sectional study, quantitative susceptibility mapping was used to investigate volume, iron concentration and total iron content of the dentate nuclei in common types of hereditary and non-hereditary degenerative ataxias. Seventy-nine patients with spinocerebellar ataxias of types 1, 2, 3 and 6; 15 patients with Friedreich’s ataxia; 18 patients with multiple system atrophy, cerebellar type and 111 healthy controls were also included. All underwent 3 T MRI and clinical assessments. For each specific ataxia subtype, voxel-based and volumes-of-interest-based group analyses were performed in comparison with a corresponding age- and sex-matched control group, both for volume, magnetic susceptiblity (indicating iron concentration) and susceptibility mass (indicating total iron content) of the dentate nuclei. Spinocerebellar ataxia of type 1 and multiple system atrophy, cerebellar type patients showed higher susceptibilities in large parts of the dentate nucleus but unaltered susceptibility masses compared with controls. Friedreich’s ataxia patients and, only on a trend level, spinocerebellar ataxia of type 2 patients showed higher susceptibilities in more circumscribed parts of the dentate. In contrast, spinocerebellar ataxia of type 6 patients revealed lower susceptibilities and susceptibility masses compared with controls throughout the dentate nucleus. Spinocerebellar ataxia of type 3 patients showed no significant changes in susceptibility and susceptibility mass. Lower volume of the dentate nuclei was found to varying degrees in all ataxia types. It was most pronounced in spinocerebellar ataxia of type 6 patients and least prominent in spinocerebellar ataxia of type 3 patients. The findings show that alterations in susceptibility revealed by quantitative susceptibility mapping are common in the dentate nuclei in different types of cerebellar ataxias. The most striking changes in susceptibility were found in spinocerebellar ataxia of type 1, multiple system atrophy, cerebellar type and spinocerebellar ataxia of type 6. Because iron content is known to be high in glial cells but not in neurons of the cerebellar nuclei, the higher susceptibility in spinocerebellar ataxia of type 1 and multiple system atrophy, cerebellar type may be explained by a reduction of neurons (increase in iron concentration) and/or an increase in iron-rich glial cells, e.g. microgliosis. Hypomyelination also leads to higher susceptibility and could also contribute. The lower susceptibility in SCA6 suggests a loss of iron-rich glial cells. Quantitative susceptibility maps warrant future studies of iron content and iron-rich cells in ataxias to gain a more comprehensive understanding of the pathogenesis of these diseases.
000902565 536__ $$0G:(DE-HGF)POF4-5251$$a5251 - Multilevel Brain Organization and Variability (POF4-525)$$cPOF4-525$$fPOF IV$$x0
000902565 7001_ $$0P:(DE-HGF)0$$aJäschke, D.$$b1
000902565 7001_ $$0P:(DE-HGF)0$$aDraganova, R.$$b2
000902565 7001_ $$0P:(DE-HGF)0$$aPfaffenrot, V.$$b3
000902565 7001_ $$0P:(DE-HGF)0$$aHulst, T.$$b4
000902565 7001_ $$0P:(DE-HGF)0$$aSteiner, K. M.$$b5
000902565 7001_ $$0P:(DE-HGF)0$$aThieme, A.$$b6
000902565 7001_ $$0P:(DE-HGF)0$$aGiordano, I. A.$$b7
000902565 7001_ $$0P:(DE-HGF)0$$aKlockgether, T.$$b8
000902565 7001_ $$0P:(DE-HGF)0$$aTunc, S.$$b9
000902565 7001_ $$0P:(DE-HGF)0$$aMünchau, A.$$b10
000902565 7001_ $$0P:(DE-Juel1)131622$$aMinnerop, Martina$$b11
000902565 7001_ $$0P:(DE-HGF)0$$aGöricke, S. L.$$b12
000902565 7001_ $$0P:(DE-HGF)0$$aReichenbach, J. R.$$b13
000902565 7001_ $$0P:(DE-HGF)0$$aTimmann, D.$$b14
000902565 773__ $$0PERI:(DE-600)3020013-1$$a10.1093/braincomms/fcab306$$n1$$pfcab306$$tBrain communications$$v4$$x2632-1297$$y2022
000902565 8564_ $$uhttps://juser.fz-juelich.de/record/902565/files/fcab306.pdf$$yOpenAccess
000902565 909CO $$ooai:juser.fz-juelich.de:902565$$pdnbdelivery$$pdriver$$pVDB$$popen_access$$popenaire
000902565 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)131622$$aForschungszentrum Jülich$$b11$$kFZJ
000902565 9131_ $$0G:(DE-HGF)POF4-525$$1G:(DE-HGF)POF4-520$$2G:(DE-HGF)POF4-500$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$9G:(DE-HGF)POF4-5251$$aDE-HGF$$bKey Technologies$$lNatural, Artificial and Cognitive Information Processing$$vDecoding Brain Organization and Dysfunction$$x0
000902565 9141_ $$y2022
000902565 915__ $$0LIC:(DE-HGF)CCBY4$$2HGFVOC$$aCreative Commons Attribution CC BY 4.0
000902565 915__ $$0StatID:(DE-HGF)0510$$2StatID$$aOpenAccess
000902565 915__ $$0StatID:(DE-HGF)0561$$2StatID$$aArticle Processing Charges$$d2020-09-12
000902565 915__ $$0StatID:(DE-HGF)0700$$2StatID$$aFees$$d2020-09-12
000902565 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2022-11-24
000902565 915__ $$0StatID:(DE-HGF)0501$$2StatID$$aDBCoverage$$bDOAJ Seal$$d2022-02-21T13:34:18Z
000902565 915__ $$0StatID:(DE-HGF)0500$$2StatID$$aDBCoverage$$bDOAJ$$d2022-02-21T13:34:18Z
000902565 915__ $$0StatID:(DE-HGF)0030$$2StatID$$aPeer Review$$bDOAJ : Blind peer review$$d2022-02-21T13:34:18Z
000902565 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2022-11-24
000902565 915__ $$0StatID:(DE-HGF)0112$$2StatID$$aWoS$$bEmerging Sources Citation Index$$d2022-11-24
000902565 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2022-11-24
000902565 9201_ $$0I:(DE-Juel1)INM-1-20090406$$kINM-1$$lStrukturelle und funktionelle Organisation des Gehirns$$x0
000902565 9801_ $$aFullTexts
000902565 980__ $$ajournal
000902565 980__ $$aVDB
000902565 980__ $$aUNRESTRICTED
000902565 980__ $$aI:(DE-Juel1)INM-1-20090406