MicroRNAs as the cause of schizophrenia in 22q11.2 deletion carriers, and possible implications for idiopathic disease: a mini-review.

[22q11.2 deletion syndrome]

The 22 q 11 .2 deletion is the strongest known genetic risk factor for schizophrenia . Research has implicated microRNA-mediated dysregulation in 22 q 11 .2 deletion syndrome (22 q 11 .2 DS ) schizophrenia -risk . Primary candidate genes are DGCR 8 (DiGeorge syndrome critical region gene 8 ), which encodes a component of the microprocessor complex essential for microRNA biogenesis , and MIR 185 , which encodes microRNA 185 . Mouse models of 22 q 11 .2 DS have demonstrated alterations in brain microRNA biogenesis , and that DGCR 8 haploinsufficiency may contribute to these alterations , e .g ., via down-regulation of a specific microRNA subset . miR-185 was the top-scoring down-regulated microRNA in both the prefrontal cortex and the hippocampus , brain areas which are the key foci of schizophrenia research . This reduction in miR-185 expression contributed to dendritic and spine development deficits in hippocampal neurons . In addition , miR-185 has two validated targets (RhoA , Cdc 42 ), both of which have been associated with altered expression levels in schizophrenia . These combined data support the involvement of miR-185 and its down-stream pathways in schizophrenia . This review summarizes evidence implicating microRNA-mediated dysregulation in schizophrenia in both 22 q 11 .2 DS -related and idiopathic cases .

Diseases
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Diseases presenting "and that dgcr8 haploinsufficiency may contribute to these alterations" symptom

22q11.2 deletion syndrome

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