Alterations in neuronal development and connectivity may contribute to the psychiatric and cognitive symptoms seen in patients with a chromosomal mutation linked to schizophrenia. A study published online in Nature Neuroscience now provides some clues to understanding the neuronal consequences of these mutations.
12% of schizophrenia cases in Caucasian populations are associated with small deletions in chromosome 22. About 30% of people with a particular microdeletion in this chromosome develop schizophrenia and many of them also have cognitive deficits.
Maria Karayiorgou and colleagues recreated this microdeletion in mice and studied neurons from the hippocampus. They report that the neurons carrying the microdeletion show reduced numbers of neuronal contacts and stunted dendrite growth. They also link these deficits to the loss of a specific enzyme that is lost with the microdeletion. This enzyme is responsible for adding fatty acid groups to certain proteins.
These findings point to alterations in neuronal proteins (specifically, a particular process called palmitoylation) as important contributors to the disease.
Maria Karayiorgou (Columbia University, New York, NY, USA)
Abstract available online.
(C) Nature Neuroscience press release.
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