131
Views
31
CrossRef citations to date
0
Altmetric
ORIGINAL INVESTIGATION

Reduced density of ADAM 12-immunoreactive oligodendrocytes in the anterior cingulate white matter of patients with schizophrenia

, , , , , , , & show all
Pages 556-566 | Received 27 Aug 2009, Accepted 17 Nov 2009, Published online: 11 Mar 2010
 

Abstract

Objectives. Abnormalities of brain white matter and oligodendroglia are replicated findings in schizophrenia research. The largely oligodendroglia-associated enzyme ADAM (A disintegrin and metalloprotease) 12 might be involved in the patho-physiology of schizophrenia, because the gene coding for human ADAM12 is located on chromosome 10q26.3, a gene locus which has been linked to schizophrenia, and some of its putative substrates are altered in schizophrenia. Methods. We studied the numerical density of ADAM12 expressing oligodendrocytes in post-mortem prefrontal brains of patients with haloperidol treated, chronic schizophrenia and matched controls. Results. A significantly reduced numerical density of ADAM12 immunoreactive oligodendrocytes was found in the white matter of the anterior cingulate cortex of schizophrenic patients. Conclusions. Although the pathophysiological implications of this finding are currently unknown, it is well conveyable that reduced ADAM12 protein contributes to a deviant metabolism of some of its substrates. These substrates are either parts of important signalling cascades (EGF, betacellulin, TGF-beta) or chemical components of myelin (neurofascin-ankyrin) known to be compromised in schizophrenia.

Acknowledgements

None.

Statement of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.