Increased Glycogen Synthase Kinase-3 beta mRNA Level in the Hippocampus of Patients with Major Depression: A Study Using the Stanley Neuropathology Consortium Integrative Databaseopen access
- Authors
- Oh, Dong Hoon; Park, Yong Chon; Kim, Seok Hyeon
- Issue Date
- Sep-2010
- Publisher
- KOREAN NEUROPSYCHIATRIC ASSOC
- Keywords
- Data mining; Glycogen synthase kinase-3 beta; Hippocampus; Major depressive disorder
- Citation
- PSYCHIATRY INVESTIGATION, v.7, no.3, pp.202 - 207
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- PSYCHIATRY INVESTIGATION
- Volume
- 7
- Number
- 3
- Start Page
- 202
- End Page
- 207
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/174215
- DOI
- 10.4306/pi.2010.7.3.202
- ISSN
- 1738-3684
- Abstract
- Objective Glycogen synthase kinase-3 beta (GSK-3 beta) has become recognized as a broadly influential enzyme affecting diverse range of biological functions, including gene expression, cellular architecture, and apoptosis. The results of previous studies suggest that GSK-3 beta activity may be increased in the brain of patients with major depressive disorders (MDD). A recent animal study reported increased GSK-3 beta messenger ribonucleic acid (mRNA) level in the hippocampus of those with depression. However, few studies have investigated GSK-3 beta activity in the brain of patients with MDD. Methods In order to test whether patients with MDD have an increase in GSK-3 beta activity in the brain compared to normal controls, we explored GSK-3 beta expression level in all brain regions by using the Stanley Neuropathology Consortium Integrative Database (SNCID), which is a web-based method of integrating the Stanley Medical Research Institute data sets. Results The level of GSK-3 beta mRNA expression in the hippocampus was significantly increased in the MDD group (n=8) compared with the control group (n=12, p<0.05). Spearman's test also reveals that GSK-3 beta mRNA expression levels were significantly correlated with nitric oxide synthase 1 (NOS1)(rho=0.70, p<0.0001) and stathmin-like 3 (STMN3)(rho=0.70, p<0.0001) in the hippocampus. Conclusion Our results correspond with the results of previous animal studies that reported increased GSK-3 beta activity in the hippocampus of those with depression. Our findings also suggest that oxidative stress-induced neuronal cell death and abnormal synaptic plasticity in the hippocampus may play important roles in the pathophysiology of major depression.
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