Yus Psychiatric Clinic

Kaohsiung, Taiwan

Yus Psychiatric Clinic

Kaohsiung, Taiwan
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Liou Y.-J.,Taipei Veterans General Hospital | Liou Y.-J.,National Yang Ming University | Chen T.-J.,Yus Psychiatric Clinic | Cheng C.-Y.,National Yang Ming University | And 5 more authors.
Current Pharmacogenomics and Personalized Medicine | Year: 2013

The involvement of neurotrophic factors, notably brain-derived neurotrophic factor (BDNF) has been suggested in the pathogenesis of major depressive disorder (MDD) and in the response of antidepressant treatment both in preclinical and clinical studies. Thus, genetic variation in human BDNF gene may be associated with MDD susceptibility and be related to treatment response to antidepressants in patients with MDD. Two hundred and eighty-eight Taiwanese patients diagnosed with MDD and 397 participants with similar mean age and gender distribution were enrolled in the study, and three markers, including rs6265 (Val66Met) in the BDNF gene were examined for their association with MDD and 4-week response to selective serotonin reuptake inhibitors (SSRI) (n = 216) using single- and haplotype-based analyses. The results showed that the Met allele of rs6265 was in allelic association with MDD. Haplotype analysis of marker combination rs2049046-rs7103411-rs6265 further indicated the association between BDNF genetic polymorphisms and MDD (global permutation p = 0.0007). Regarding 4-week SSRI treatment response and controlling the effect of relevant covariates using logistic regression, the heterozygotes of rs7103411 and rs6265 had higher treatment responder percentage than their homozygous analogs. Furthermore, MDD patients carrying AGA-TAG diplotype tended to be the responders to 4-week SSRIs treatment compared with the non-AGA-TAG diplotype carriers (corrected p= 0.048). One strength of our study is the relatively large sample size. Our findings suggest that BDNF may be a susceptibility gene for MDD, and may also confer a heterosis effect for antidepressant treatment response. © 2013 Bentham Science Publishers.


Lee T.-W.,Chang Gung Memorial Hospital | Lee T.-W.,Chang Gung University | Yu Y.W.-Y.,Yus Psychiatric Clinic | Hong C.-J.,Taipei Veterans General Hospital | And 6 more authors.
Brain Topography | Year: 2012

The epsilon4 allele of the Apolipoprotein E (ApoE) gene has been linked to various neurological conditions and the aging process in the elderly. However, evidence has suggested that the influence of ApoE epsilon4 may commence in early life. This study examined the modulatory effects of ApoE epsilon4 on regional neural activity as well as inter-regional neural interactions in a young population aged 19-21. Blood samples and resting state eyes-closed EEG signals were collected from 265 healthy females, and stratified into two groups: epsilon4 carriers and non-carriers. The values of the log-transformed mean power of 18 electrodes and the mutual information of 20 channel pairs across delta, theta, alpha and beta frequencies were analyzed. Our connectivity analysis was based on information theory, which combined Morlet wavelet transform and mutual information calculation. Between-group statistics were performed by independent ttest. We notice a consistent trend across the brain, in which ApoE epsilon4 carriers possess lower regional power at the alpha band. The epsilon4 allele is also associated with lower regional power at the theta frequency in the left frontal and posterior brain regions. Functional connectivity analyses reveal a right-lateralized network that differentiates epsilon4 carriers and non-carriers, with lower connectivity strengths for the former. Our tonic EEG analyses complement those of previous reports in that the ApoE epsilon4 allele has a negative impact on regional neural synchronization and inter-regional neural interaction. © Springer Science+Business Media, LLC 2012.


Lee T.-W.,Chang Gung Memorial Hospital | Lee T.-W.,Chang Gung University | Yu Y.W.-Y.,Yus Psychiatric Clinic | Chen M.-C.,Kai Suan Psychiatric Hospital | Chen T.-J.,E DA Hospital
Journal of Affective Disorders | Year: 2011

Background: Diagnosis and treatment rely on symptom criteria in modern psychiatry. However, the cortical mechanisms of symptomatology in major depressive disorder (MDD) are still not clear. This study examined neural correlates of symptom clusters of MDD by electroencephalography (EEG). Methods: Resting state eye-closed EEG signals were recorded in 196 depressive patients. Quantitative EEG (qEEG) of regional power, coherence and power series correlation across delta, theta, alpha and beta frequencies were used to correlate with overall depression severity evaluated by the Hamilton Depression Rating Scale (HDRS). Further, statistical comparisons between patients with high vs. low qEEG indices (median-split) were undertaken regarding symptom severity of core depression, sleep, activity, psychic anxiety, somatic anxiety, and delusion. Results: None of the qEEG indices significantly correlated with overall depression severity or differentiated symptom severity of core depression, sleep, activity and psychic anxiety. A higher symptom severity of somatic anxiety was associated with higher regional power over widespread cortical regions and lower strengths at bi-temporal, temporo-parietal and fronto-parietal connections. A higher symptom severity of delusion was associated with higher regional power in the frontal and temporal regions, and lower strengths at inter-hemispheric (frontal, temporal and parietal) and fronto-temporo-parietal connections. Limitations: Our EEG recording with sampling rate of 128 Hz and 20 electrodes may provide restricted spatial and temporal precision. Conclusions: Our results suggest that cortical mechanisms play important roles in the symptom manifestation of cognitive distortion (sub-score of delusion) and somatic anxiety in MDD. Our findings further imply that psychic anxiety and somatic anxiety are distinct entities. © 2010 Elsevier B.V. All rights reserved.


Liou Y.-J.,Taipei Veterans General Hospital | Liou Y.-J.,National Yang Ming University | Chen C.-H.,Academia Sinica, Taiwan | Chen C.-H.,China Medical University at Taichung | And 9 more authors.
PLoS ONE | Year: 2012

Objectives: The forced swim test (FST) is a commonly used model to predict antidepressant efficacy. Uncovering the genetic basis of the model may unravel the mechanism of antidepressant treatment. Methods: FVB/NJ (FVB) and C57BL/6J (B6) were first identified as the response and non-response strains to fluoxetine (a serotonin-specific reuptake inhibitor antidepressant) treatment in the mouse FST. Simple-interval (SIM) and composite-interval (CIM) mappings were applied to map the quantitative trait loci (QTLs) of the anti-immobility effect of fluoxetine in FST (FSTFLX) in 865 male B6×FVB-F2 mice. The brain mRNA expressions of the gene with the maximum QTL-linkage signal for FSTFLX after the FST were compared between B6 and FVB mice and also compared between fluoxetine and saline treatment. The association of the variants in the human homologue of the mouse FSTFLX-QTL gene with major depressive disorder (MDD) and antidepressant response were investigated in 1080 human subjects (MDD/control = 582/498). Results: One linkage signal for FSTFLX-QTL was detected at an intronic SNP (rs6215396) of the mouse Zfp326 gene (maximal CIM-LOD = 9.36). The Zfp326 mRNA expression in the FVB thalamus was significantly down-regulated by fluoxetine in the FST, and the higher FVB-to-B6 Zfp326 mRNA expressions in the frontal cortex, striatum and hypothalamus diminished after fluoxetine treatment. Two coding-synonymous SNPs (rs2816881 and rs10922744) in the human homologue of Zfp326, ZNF326, were significantly associated with the 8-week antidepressant treatment response in the MDD patients (Bonferroni-corrected p = 0.004-0.028). Conclusions: The findings suggest the involvement of the Zfp326 and ZNF326 genes in antidepressant treatment response. © 2012 Liou et al.


Lee T.-W.,Chang Gung Memorial Hospital | Lee T.-W.,Chang Gung University | Yu Y.W.-Y.,Yus Psychiatric Clinic | Hong C.-J.,Taipei Veterans General Hospital | And 6 more authors.
Brain Research | Year: 2011

The catechol-O-methyl-transferase (COMT) gene has been linked to a wide spectrum of human phenotypes, including cognition, affective response, pain sensitivity, anxiety and psychosis. This study examined the modulatory effects of COMT Val158Met on neural interactions, indicated by connectivity strengths. Blood samples and resting state eyes-closed EEG signals were collected in 254 healthy young females. The COMT Val158Met polymorphism was decoded into 3 groups: Val/Val, Val/Met and Met/Met. The values of mutual information of 20 frontal-related channel pairs across delta, theta, alpha and beta frequencies were analyzed based on the time-frequency mutual information method. Our one-way ANOVA analyses revealed that the significant connection-frequency pairs were relatively left lateralized (P < 0.01) and included F7-T3 and F7-C3 at delta frequency, and F3-F4, F7-T3, F7-C3, F7-P3, F3-C3, F3-F7 and F4-F8 at theta frequency. The F-test at F7-T3 and F7-C3 theta surpassed the statistical threshold of P < 0.003 (after Bonferroni correction). For all the above connection-frequency pairs, there was a dose-dependent trend in the connectivity strengths of the alleles as follows: Val/Val > Val/Met > Met/Met. Our analyses complemented previous literature regarding neural modulation by the COMT Val158Met polymorphism. The implication to the pathogenesis in schizophrenia was also discussed. Further studies are needed to clarify whether there is gender difference on this gene-brain interaction. © 2010 Elsevier B.V. All rights reserved.


Lee T.-W.,Laureate Institute for Brain Research | Wu Y.-T.,National Yang Ming University | Yu Y.W.-Y.,Yus Psychiatric Clinic | Chen M.-C.,Kai Suan Psychiatric Hospital | And 2 more authors.
Psychiatry Research - Neuroimaging | Year: 2011

Predicting treatment response in major depressive disorder (MDD) has been an important clinical issue given that the initial intent-to-treat response rate is only 50 to 60%. This study was designed to examine whether functional connectivity strengths of resting EEG could be potential biomarkers in predicting treatment response at 8. weeks of treatment. Resting state 3-min eyes-closed EEG activity was recorded at baseline and compared in 108 depressed patients. All patients were being treated with selective serotonin-reuptake inhibitors. Baseline coherence and power series correlation were compared between responders and non-responders evaluated at the 8th week by Hamilton Depression Rating Scale. Pearson correlation and receiver operating characteristic (ROC) analyses were applied to evaluate the performance of connectivity strengths in predicting/classifying treatment responses. The connectivity strengths of right fronto-temporal network at delta/theta frequencies differentiated responders and non-responders at the 8th week of treatment, such that the stronger the connectivity strengths, the poorer the treatment response. ROC analyses supported the value of these measures in classifying responders/non-responders. Our results suggest that fronto-temporal connectivity strengths could be potential biomarkers to differentiate responders and slow responders or non-responders in MDD. © 2011 Elsevier Ireland Ltd.

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