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Citation |
Devaraju P, Zakharenko SS. Bioessays 2017; 39(2): e101600177. |
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Affiliation |
Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN, USA. |
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Copyright |
(Copyright © 2017, International Council of Scientific Unions, Publisher John Wiley and Sons) |
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DOI |
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PMID |
28044359 |
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Abstract |
Mitochondrial ATP synthesis, calcium buffering, and trafficking affect neuronal function and survival. Several genes implicated in mitochondrial functions map within the genomic region associated with 22q11.2 deletion syndrome (22q11DS), which is a key genetic cause of neuropsychiatric diseases. Although neuropsychiatric diseases impose a serious health and economic burden, their etiology and pathogenesis remain largely unknown because of the dearth of valid animal models and the challenges in investigating the pathophysiology in neuronal circuits. Mouse models of 22q11DS are becoming valid tools for studying human psychiatric diseases, because they have hemizygous deletions of the genes that are deleted in patients and exhibit neuronal and behavioral abnormalities consistent with neuropsychiatric disease. The deletion of some 22q11DS genes implicated in mitochondrial function leads to abnormal neuronal and synaptic function. Herein, we summarize recent findings on mitochondrial dysfunction in 22q11DS and extend those findings to the larger context of schizophrenia and other neuropsychiatric diseases. Language: en |