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

Hagemeyer, N., Goebbels, S., Papiol, S., Kästner, A., Hofer, S., Begemann, M., et al. (2012). A myelin gene causative of a catatonia-depression syndrome upon aging. EMBO Molecular Medicine, 4(6), 528-539. doi:10.1002/emmm.201200230.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-000F-9B65-B Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0027-C69D-9
Genre: Journal Article

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 Creators:
Hagemeyer, N., Author
Goebbels, S., Author
Papiol, S., Author
Kästner, A., Author
Hofer, S.1, Author              
Begemann, M., Author
Gerwig, U., Author
Boretius, S.1, Author              
Wieser, G. L., Author
Ronnenberg, A., Author
Gurvich, A., Author
Heckers, S. H., Author
Frahm, J.1, Author              
Nave, K. A., Author
Ehrenreich, H., Author
Affiliations:
1Biomedical NMR Research GmbH, MPI for biophysical chemistry, Max Planck Society, ou_578634              

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Free keywords: Anxiety; axonal degeneration; diffusion tensor imaging; low-grade inflammation; social withdrawal
 Abstract: Severe mental illnesses have been linked to white matter abnormalities, docu- mented by postmortem studies. However, cause and effect have remained difficult to distinguish. CNP (2 0 ,3 0 -cyclic nucleotide 3 0 -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 strik- ingly similar in Cnp heterozygous mice and patients with mental disease carrying the AAgenotypeat CNP SNPrs2070106.The characteristicfeatures inbothspecies with their partial CNP ‘loss-of-function’ genotype are best described as ‘catatonia- depression’ syndrome. As a consequence of perturbed CNP expression, mice show secondary low-grade inflammation/neurodegeneration. Analogously, in man, dif- fusion 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.

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Language(s): eng - English
 Dates: 2012-04-042012-06
 Publication Status: Published in print
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 Rev. Method: Peer
 Identifiers: DOI: 10.1002/emmm.201200230
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Title: EMBO Molecular Medicine
Source Genre: Journal
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Pages: - Volume / Issue: 4 (6) Sequence Number: - Start / End Page: 528 - 539 Identifier: -