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A myelin gene causative of a catatonia-depression syndrome upon aging

dc.contributor.authorHagemeyer, Nora
dc.contributor.authorGoebbels, Sandra
dc.contributor.authorPapiol, Sergi
dc.contributor.authorKästner, Anne
dc.contributor.authorHofer, Sabine
dc.contributor.authorBegemann, Martin
dc.contributor.authorGerwig, Ulrike C.
dc.contributor.authorBoretius, Susann
dc.contributor.authorWieser, Georg L.
dc.contributor.authorRonnenberg, Anja
dc.contributor.authorGurvich, Artem
dc.contributor.authorHeckers, Stephan H.
dc.contributor.authorFrahm, Jens
dc.contributor.authorNave, Klaus-Armin
dc.contributor.authorEhrenreich, Hannelore
dc.date.accessioned2012-07-16T10:25:10Z
dc.date.available2012-07-16T10:25:10Z
dc.date.issued2012
dc.identifier.citationHagemeyer, Nora; Goebbels, Sandra; Papiol, Sergi; Kästner, Anne; Hofer, Sabine; Begemann, Martin; Gerwig, Ulrike C.; Boretius, Susann; Wieser, Georg L.; Ronnenberg, Anja; Gurvich, Artem; Heckers, Stephan H.; Frahm, Jens; Nave, Klaus-Armin; Ehrenreich, Hannelore (2012): A myelin gene causative of a catatonia-depression syndrome upon aging - EMBO Molecular Medicine, Vol. 4, Nr. 6, p. 528-539
dc.relation.ISSN1757-4684
dc.identifier.urihttp://resolver.sub.uni-goettingen.de/purl?gs-1/7776
dc.description.abstractSevere mental illnesses have been linked to white matter abnormalities, documented by postmortem studies. However, cause and effect have remained difficult to distinguish. CNP (20,30-cyclic nucleotide 30-phosphodiesterase) is among the oligodendrocyte/myelin-associated genes most robustly reduced on mRNA and protein level in brains of schizophrenic, bipolar or major depressive patients. This suggests that CNP reduction might be critical for a more general disease process and not restricted to a single diagnostic category. We show here that reduced expression of CNP is the primary cause of a distinct behavioural phenotype, seen only upon aging as an additional ‘pro-inflammatory hit’. This phenotype is strikingly similar in Cnp heterozygous mice and patients with mental disease carrying the AA genotype at CNP SNP rs2070106. The characteristic features in both species with their partial CNP ‘loss-of-function’ genotype are best described as ‘catatoniadepression’ syndrome. As a consequence of perturbed CNP expression, mice show secondary low-grade inflammation/neurodegeneration. Analogously, in man, diffusion tensor imaging points to axonal loss in the frontal corpus callosum. To conclude, subtle white matter abnormalities inducing neurodegenerative changes can cause/amplify psychiatric diseases.
dc.language.isoeng
dc.relationinfo:eu-repo/grantAgreement/EC/FP7/201535/EU//NGIDD
dc.rightsopenAccess
dc.subjectanxiety; axonal degeneration; diffusion tensor imaging; low-grade inflammation; social withdrawal
dc.titleA myelin gene causative of a catatonia-depression syndrome upon aging
dc.typejournalArticle
dc.identifier.doi10.1002/emmm.201200230
dc.type.versionpublishedVersion
dc.bibliographicCitation.volume4
dc.bibliographicCitation.issue6
dc.bibliographicCitation.firstPage528
dc.bibliographicCitation.lastPage539
dc.type.subtypejournalArticle
dc.identifier.pmid22473874
dc.relation.euprojectNGIDD
dc.description.statuspeerReviewed
dc.bibliographicCitation.journalEMBO Molecular Medicine


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