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Chen-Jee Hong

Publications and source records attributed to Chen-Jee Hong.

At least 55 records · Page 3Linked to original sources
PubMed2004

Possible association between serotonin transporter promoter region polymorphism and extremely violent crime in Chinese males.

The neurotransmitter, serotonin, has been implicated in aggressive behavior. The serotonin transporter (5-HTT), which reuptakes serotonin into the nerve terminal, plays a critical role in the regulation of serotonergic function. Previous western reports have demonstrated that the low-activity short (S) allele of the 5-HTT gene-linked polymorphic-region (5-HTTLPR) polymorphism is associated with aggressive behavior and associated personality traits. In the present study, we investigated this 5-HTTLPR genetic polymorphism in a group of Chinese males who had been convicted for extremely violent crime (n = 135) and a normal control group (n = 111). The proportion of S-allele carriers was significantly higher in the criminal group than in the controls (p = 0.006). A significant association was not demonstrated for the relationship between the 5-HTTLPR polymorphism and antisocial personality disorder, substance abuse or alcohol abuse in the criminal group. Our findings demonstrate that carriage of the low-activity S allele is associated with extremely violent criminal behavior in Chinese males, and suggests that the 5-HTT may be implicated in the mechanisms underlying violent behaviors.

Adult↗
PubMed2004

Association analysis for MAOA gene polymorphism with long-latency auditory evoked potentials in healthy females.

The components of auditory evoked potentials (AEPs) have been demonstrated to be heritable and to be influenced by different neurotransmitter activities such as serotonin or dopamine. Monoamine oxidase A (MAOA) is a mitochondrial enzyme involved in the degradation of dopamine, serotonin and norepinephrine. We examined the potential association of the functional 30-bp repeat MAOA gene-linked polymorphism region (MAOA-LPR) in 234 normal young Chinese females. The results demonstrated that there is no association for MAOA-LPR polymorphism and AEP components. Our negative findings suggested that this genetic polymorphism does not play a major role in the modulation of AEPs in normal young females, but we could not exclude that other polymorphisms of the MAOA gene affect AEP components. Further exploration of the other polymorphisms of the MAOA gene and multiple interactions of the polymorphisms in various neurotransmitter systems may be needed in future studies.

Adult↗
PubMed2004

Association analysis for the C-1019G promoter variant of the 5-HT1A receptor gene with auditory evoked potentials in major depression.

Involvement of the serotonergic system in N1 and P2 components of auditory evoked potentials (AEPs) has been implicated. Moreover, studies have indicated the presence of heritability in the genesis of AEP components. The serotonin 1A (5-HT1A) receptor gene is a strong candidate for N1 and P2 components of the AEPs because 5-HT1A receptor regulates the firing of serotonergic neurons. The present study tested the hypothesis that the 5-HT1A promoter genetic polymorphism (C-1019G) is associated with N1 and P2 components of AEPs in unmedicated major depression patients. The sample consisted of 221 Chinese patients (mean age: 44.3 years; male/female: 93/128) diagnosed with major depression. AEPs and 5-HT1A genotyping were done for each patient. Patients with the C/C genotype had a significantly shorter P2 latency when compared with C/G or G/G genotype patients (p = 0.049), and the difference in P2 latency was significant among the 5-HT1A genotype groups in male patients (p = 0.031) but not in female patients (p = 0.398). These findings suggest that this 5-HT1A polymorphism may affect AEP P2 latency in a gender-dependent manner. Further studies with other genetic polymorphisms in the serotonergic system may help to clarify the relation between serotonergic function and AEP components.

Adolescent↗
PubMed2003

Brain-derived neurotrophic factor (BDNF) Val66Met polymorphisms in Parkinson's disease and age of onset.

Given the implications with respect to neuronal survival and the decreased level of the protein in the striatal region in Parkinson's disease (PD), brain-derived neurotrophic factor (BDNF) may be a candidate gene conferring susceptibility to PD. In a recent study of a Japanese population, a functional BDNF Val66Met polymorphism was associated with PD, however, an analogous investigation of a western population did not replicate this finding. In the present study of a Chinese sample, we have investigated the associations between the BDNF polymorphism and susceptibility to PD and PD onset age. The distribution of the BDNF genotypes and alleles did not differ significantly comparing PD patients and controls. Further, the onset age was not significantly different comparing the three BDNF genotype groups. Thus, our negative findings suggest that it is unlikely that the BDNF Val66Met polymorphism plays a major role in the pathogenesis of PD in the Chinese population. Other BDNF genetic variants, and the association of these variants with PD symptomatology or treatment response, may merit further investigation.

Age of Onset↗
PubMed2003

No association of tumor necrosis factor alpha gene polymorphisms with schizophrenia or response to clozapine.

Tumor necrosis factor alpha (TNF-alpha), a potent immunomodulator and proinflammatory cytokine, has been implicated in schizophrenia pathogenesis and clozapine response. Two studies have established an association between schizophrenia and the TNF-alpha gene -308G/A polymorphism; however, both increased and decreased -308A allele frequency have been reported in two analogous investigations. The present study examined the hypothesis that the TNF-alpha gene -308G/A polymorphism confers susceptibility to schizophrenia in 205 patients with schizophrenia compared with 192 controls. A subgroup of 99 clozapine-treated schizophrenia patients was also tested for the genetic effects of this polymorphism, as evidenced by clinical manifestation, and clozapine-related therapeutic outcome and body-weight change. The results of these investigations suggest that the TNF-alpha gene -308G/A variants do not play a major role in susceptibility to, clinical manifestations for, or clozapine response in, schizophrenia.

Adult↗
PubMed2003

Association study of a brain-derived neurotrophic-factor genetic polymorphism and major depressive disorders, symptomatology, and antidepressant response.

Preclinical studies have shown that brain-derived neurotrophic factor (BDNF) may be involved in both antidepressant action and the pathophysiology of major depressive disorder (MDD). The present study tested the hypothesis that the BDNF-gene Val66Met polymorphism is associated with MDD, its clinical manifestations, and antidepressant response. To elucidate a genetic predisposition of MDD, we studied BDNF-gene Val66Met polymorphism in 152 MDD patients in 255 normal controls. We also examined the association of this polymorphism and fluoxetine therapeutic response in 110 MDD patients who received a 4-week fluoxetine treatment. No significant differences were demonstrated for the genotype or allele frequency of the BDNF polymorphism comparing the MDD and control groups. Further, no significant differences were noted comparing the three-genotype groups for depressive-cluster symptoms. However, a trend (P = 0.086) to improved 4-week-fluoxetine antidepressant response was demonstrated for heterozygous patients in comparison to homozygous analogs. This finding suggests the BDNF polymorphism investigated plays no major role in the pathogenesis of MDD.

Adult↗
PubMed2003

An association study of a brain-derived neurotrophic factor Val66Met polymorphism and clozapine response of schizophrenic patients.

A growing body of evidence suggests the involvement of brain-derived neurotrophic factor (BDNF) in both antipsychotic action and schizophrenia pathogenesis. The present study tested the hypothesis that the BDNF-gene Val66Met polymorphism is associated with schizophrenia and clozapine's therapeutic response. To identify any genetic predisposition to schizophrenia, we studied the BDNF-gene Val66Met polymorphism in 93 schizophrenic patients and 198 normal controls. Statistical analysis was used to test the association between this polymorphism and clozapine response the schizophrenic group. A trend (P=0.055) was demonstrated between genetic predisposition and Val66Met genotypes in 93 schizophrenic patients, especially for those with good response to clozapine (P=0.023). No significant difference in clozapine therapeutic response was demonstrated comparing the three Val66Met-genotype subgroups. Our finding suggests that this BDNF-gene Val66Met polymorphism may be related to schizophrenia pathogenesis in patients responsive to clozapine treatment.

Adult↗
PubMed2003

Lack of association between the interleukin-1alpha gene C(-889)T polymorphism and Alzheimer's disease in a Chinese population.

Interleukin 1A (IL-1A), a potent proinflammatory cytokine, has been implicated in the pathogenesis of Alzheimer's disease (AD). Several recent studies have shown that a polymorphism in the IL-1A locus -889 was associated with AD risk and onset age, however, other studies were not able to replicate these findings. In this investigation, the IL-1A C(-889)T polymorphism has been analyzed for a Chinese population of 234 AD patients and 170 controls. There were no significance differences in IL-1A genotype or allele frequencies comparing the AD cases and controls, even after stratification for age of onset and adjustment for apolipoprotein E genotype. The results reveal that it is not likely that the IL-1A C(-889)T polymorphism is involved in AD pathogenesis in the Chinese population. Further studies of the associations between other IL-1A genetic polymorphisms and AD are needed to fully elaborate the involvement of this gene in AD.

Aged↗
PubMed2003

Association study of the interleukin-1 beta (C-511T) genetic polymorphism with major depressive disorder, associated symptomatology, and antidepressant response.

Proinflammatory cytokines, including interleukin (IL)-1beta, are suggested to have a role in the pathogenesis of major depressive disorder (MDD) and be related to the therapeutic effects of antidepressants. To elucidate a genetic predisposition of MDD, we studied biallelic polymorphism in the promoter region (position -511) of the IL-1beta gene in 157 patients with MDD and in 112 controls. We also examined the association of this polymorphism and fluoxetine therapeutic response in 119 MDD patients who received a 4-week fluoxetine treatment. No significant difference was found in the genetic polymorphism between MDD patients and controls. However, MDD patients who were homozygous for the -511T allele of the IL-1beta gene had a trend of less severity of depressive symptoms and more favorable fluoxetine therapeutic response than -511C carriers. Further study with a larger sample is needed to clarify the role of the IL-1beta genetic polymorphisms in the symptoms and treatment effects in MDD.

Adolescent↗
PubMed2003

Dopamine receptor hetero-oligomerization: a hypothesis for behavioral sensitization to psychostimulants.

Repeated psychostimulant pretreatment can induce behavioral sensitization. Many previous studies have demonstrated that receptors of the dopamine and other neurotransmitter systems are involved in the sensitization process, however, the precise mechanism of this interaction is still unknown. We propose the hypothesis that oligomerization of the dopamine receptors and analogs from other neurotransmitter systems may contribute, at least in part, to psychostimulant-induced behavioral sensitization. Psychostimulant exposure can enhance central dopamine release, which can increase oligomerization of the dopamine receptors with their analogs. Receptor oligomerization can enhance the functional properties of the receptors and affect receptor degradation, which may be related to the behavioral augmentation which characterizes the sensitized state and produces the persistence of behavioral sensitization. The proposed receptor hetero-oligomerization model may provide a new direction in the exploration of the functionally critical sensitization phenomenon.

Amphetamines↗
PubMed2003

Association study of oestrogen receptor alpha gene polymorphism and suicidal behaviours in major depressive disorder.

OBJECTIVE: Gender comparison in epidemiological studies has consistently demonstrated a greater prevalence for major depressive disorders (MDD) in females. Several lines of evidence have implicated oestrogen pathways in this gender difference. Furthermore, there is evidence that attempted suicides are more frequent in women. A population-based association study was used to test the hypothesis that the genetic variants ( II and I polymorphisms) of the oestrogen receptor alpha gene (ER-alpha) confer susceptibility to MDD. METHODS: The ER-alpha was genotyped for 154 patients with MDD and 226 controls in a Chinese population. RESULTS: Statistical analysis showed a significant difference in the II genotype and allele frequencies between the female MDD patients and the female controls ( P=0.010 and P=0.004, respectively). However, no significant differences in ER-alpha genotype or allele frequencies were found between male MDD patients and male controls. Furthermore, the ER-alpha genotypes were not associated with suicide-attempt history for MDD cases. CONCLUSIONS: Our results suggest that the ER-alpha may play a role in the susceptibility of MDD in females.

Base Sequence↗
PubMed2003

Association analysis for dopamine D3 receptor, dopamine D4 receptor and dopamine transporter genetic polymorphisms and P300 event-related potentials for normal young females.

OBJECTIVE: It has been demonstrated that the P300 components, a positive event-related potential, are heritable and are influenced by dopaminergic activity. We tested the genetic effects of the dopaminergic system in P300 components by association study. METHODS: In a sample population consisting of 120 normal young Han-Chinese females, we explored the association between the P300 components, and, the genetic polymorphisms including the dopamine D3 receptor (serine-to-glycine polymorphism in exon I), the dopamine D4 receptor (variable number tandem repeat polymorphism in exon III), and the dopamine transporter (variable number tandem repeat polymorphism in promoter region). RESULTS: No associations were demonstrated between the polymorphisms of these three genes and the P300 components. CONCLUSIONS: Our negative findings suggest that these genetic polymorphisms do not play a major role in the modulation of P300 event-related potentials.

Adult↗
PubMed2003

Association analysis for neuronal nitric oxide synthase gene polymorphism with major depression and fluoxetine response.

Nitric oxide (NO) is produced from its precursor L-arginine by the enzyme NO synthase (NOS), which includes at least three distinct isoforms - neuronal (nNOS), endothelial, and inducible NOS. Recent studies have implicated NOS in the mechanism that underlies the therapeutic efficacy of antidepressant medication. In addition, major depressive disorder (MDD) patients were found to have significantly higher plasma nitrate concentrations than normal subjects, an index of NO production, in comparison to normal subjects. In a population-based association study, we tested the hypothesis that the nNOS C276T polymorphism confers susceptibility to MDD. We also examined the association between this polymorphism and therapeutic fluoxetine response in 114 MDD patients who underwent a 4-week fluoxetine treatment. The results demonstrate that the nNOS variants are found at similar frequencies in MDD patients and healthy control subjects. Further, we did not discover any genetic variants that influenced the fluoxetine response in MDD patients treated with fluoxetine. Our findings suggest that this nNOS C276T polymorphism does not play a major role in the susceptibility to, or fluoxetine response in, MDD. However, the association between other NOS variants and MDD or antidepressant response, including sexual dysfunction, may warrant further investigation.

Adult↗
PubMed2003

Association study of serotonin transporter gene VNTR polymorphism and mood disorders, onset age and suicide attempts in a Chinese sample.

The human serotonin transporter (5-HTT) gene is an important candidate for the pathogenesis of mood disorders. Associations have been reported between a variable-number tandem-repeat polymorphism in intron 2 of the serotonin transporter gene (5-HTTVNTR) and mood disorders in a number of studies of Western and Chinese populations. However, no such relationships have been determined in other analogous research. To replicate these positive findings in a Chinese population and to determine the association between onset age of bipolar disorder and 5-HTTVNTR, we investigated the prevalence of this polymorphism in an independent Chinese population (83 bipolar disorder patients, 77 major depressive disorder patients and 169 controls), demonstrating no significant association between the 5-HTTVNTR polymorphism and mood disorders or age at onset. Further, no association was demonstrated between this polymorphism and suicidal history in mood disorder patients. These negative findings suggest that 5-HTTVNTR does not play a major role in the pathogenesis of mood disorder in Chinese populations.

Adult↗
PubMed2003

Allelic variants of the tryptophan hydroxylase (A218C) and serotonin 1B receptor (A-161T) and personality traits.

Human personality traits have a considerable hereditary component, and central serotonergic activity is implicated in the personality factors of the Tridimensional Personality Questionnaire (TPQ). Our population-based association study tested the hypothesis that the tryptophan hydroxylase (TPH) A218C and serotonin 1B receptor (HTR1B) A-161T polymorphisms were associated with TPQ personality trait scores in a sample population of 209 young healthy Chinese. No significant differences were demonstrated comparing scores of subjects bearing different TPH or HTR1B genotypes; however, a trend for difference in the novelty seeking score comparing TPH genotype groups was determined for the male population. Our negative findings suggest that the TPH A218C and HTR1B polymorphisms do not play major roles in the determination of TPQ personality traits.

Adult↗
PubMed2003

Association of muscarinic m1 receptor genetic polymorphisms with psychiatric symptoms and cognitive function in schizophrenic patients.

OBJECTIVE: The cholinergic system is important in the search for the pathophysiology of schizophrenia due to its role in cognitive function, interaction with the dopamine system in brain regions relevant to schizophrenia, side effects of antipsychotic medication and potential antipsychotic effect of muscarinic receptor antagonists. This study investigated the association of type I muscarinic receptor (CHRM1) genetic polymorphisms with the clinical characteristics of chronic schizophrenic inpatients. METHODS: We determined the genotype of CHRM1 genetic polymorphisms in 243 schizophrenic patients hospitalized in chronic care wards. Psychotic symptoms were assessed using the Brief Psychiatric Rating Scale (BPRS), and cognitive function was assessed using the Folstein Mini-Mental Status Examination (MMSE) test. Sixty of the 243 subjects also completed the Wisconsin Card Sorting Test (WCST). RESULTS: There was a significant difference in the number of correct responses and the percentage of perseverative errors in the WCST in the CHRM1 C267A genotype group of schizophrenia patients. There was no significant association between age at onset, chlorpromazine equivalents, BPRS scores, MMSE or schizophrenia per se in patients with the CHRM1 C267A genotype. The full exon of the CHRM1 gene was screened out with single-strand conformation polymorphism, and 2 single nucleotide polymorphisms (C267A and C1353T) were identified in our patients and control subjects. These 2 single nucleotide polymorphisms were linked together without exception. CONCLUSION: This study demonstrated that in schizophrenic patients, the heterozygote group of CHRM1 C267A polymorphism (267C/A) had more correct responses and less perseverative errors on the WCST performance than the 267C/C homozygote group, implicating that this polymorphism may be related to prefrontal cortical function. Our results also suggested that the C267A polymorphism plays no major role in the susceptibility to and clinical manifestations of schizophrenia.

Adolescent↗