Journal
NEUROREPORT
Volume 18, Issue 1, Pages 57-60Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/WNR.0b013e32800fefd7
Keywords
cytosine methylation; epigenetic; GABAergic neurons; homocysteine; methionine; schizophrenia
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Funding
- NIMH NIH HHS [R01MH70855, R01MH6262A, R01MH71667] Funding Source: Medline
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Prefrontal cortex (Brodmann's area 9) levels of the methyl donor S-adenosyl methionine were increased by about two-fold in schizophrenia and bipolar disorder patients, but not in unipolar depressed patients compared with nonpsychiatric subjects from the Stanley Foundation Neuropathology Consortium (Bethesda, Maryland, USA). Neither age, brain weight and pH, hemisphere, post-mortem interval, disease onset/duration, nor cumulative dose of fluphenazine affected S-adenosyl methionine content. In schizophrenia and bipolar disorder patients, the increase of S-adenosyl methionine is associated with an overexpression of DNA m ethyltransfe rase-I mRNA in Brodmann's area 9 GABAergic neurons. Hence, the increased expression of S-adenosyl methionine and DNA methyltransferase-I may contribute to promoter cytosine 5-methylation and to downregulation of the expression of mRNAs encoding for reelin and GAD67 in cortical GABAergic neurons of schizhophrenia and bipolar disorder patients.
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