Biomedical subjects

C J Hong

Publications and source records attributed to C J Hong.

At least 37 records · Page 2Linked to original sources

PubMed2001

Genetic association analysis of alpha-1-antichymotrypsin polymorphism in Parkinson's disease.

alpha(1)-Antichymotrypsin (ACT) gene has been suggested as a susceptibility factor for Parkinson's disease (PD) and might be related to the onset of PD. We replicated these findings in a Chinese population. The results demonstrated that the ACT genotypic and allelic distributions showed no significant differences between the PD patient and the control groups. The age at onset was younger in the heterozygotes than in the homozygotes (p = 0.042). We suggest that the ACT polymorphism might play some role in the pathogenesis of PD, especially in the onset.

Age of Onset↗

PubMed2001

No association between tryptophan hydroxylase gene polymorphism and Alzheimer's disease.

Serotonergic dysfunction is implicated in Alzheimer's disease (AD) on the basis of studies of serotonin and its metabolite in postmortem specimens and CSF. There were also reports on association of a tryptophan hydroxylase (TPH) intron 7 variant and CSF 5-hydroxyindoleacetic acid concentrations. These suggested TPH might be a candidate to study for possible involvement in AD. Using a case-control association approach, we studied the TPH polymorphism in 150 subjects with AD and 100 controls. There were no significant differences in genotype or allele frequencies between controls and AD patients. The negative findings suggested that this TPH polymorphism has no major effect on the development of AD. However, the genetic variation of the TPH gene related to the symptomatology of AD deserves further investigation.

Aged↗

PubMed2001

Association analysis of a functional catechol-o-methyltransferase gene polymorphism in schizophrenic patients in Taiwan.

The catechol-O-methyltransferase (COMT) gene was thought to be a candidate gene for schizophrenia because of its role in inactivating dopamine. This study examined the relationship between a functional polymorphism (val158met) of the COMT gene, schizophrenia and its associated behaviors. One hundred and ninety-eight Chinese schizophrenic patients and 188 controls were genotyped by polymerase chain reaction restriction fragment length polymorphism. Of the schizophrenic patients, 72 had a history of violence and 62 had a history of suicide attempts. The results failed to show significant association between val158met polymorphism and schizophrenia, violence or suicide. However, our results showed a significant difference in age at disease onset among different genotypes (F = 5.501, p = 0.005).

Adult↗

PubMed2001

Association study of a nicotinic receptor variant with schizophrenic disorders.

Nicotine acetylcholine receptors (nAChRs) are implicated in the pathogenesis of schizophrenia because the prevalence of smoking among schizophrenic patients is extraordinarily high, and nicotine has been demonstrated to improve some psychophysiological dysfunction in schizophrenics. In addition, recent studies have suggested linkage of the alpha(7) nAChR gene region in families of schizophrenics. In a population-based association study, we tested the hypothesis that the allelic variant, with a 2-bp deletion, of the human alpha(7) nAChR gene confers susceptibility to schizophrenic disorders. We genotyped alpha(7) nAChR in 146 patients with schizophrenic disorders and 151 controls. The results showed no significant difference in genotype or allele frequencies between schizophrenic patients and control subjects. This suggests that alpha(7) nAChR 2-bp deletion plays no major role in the pathogenesis of schizophrenic disorders. Other nAChR variants in schizophrenic disorders may need further investigation.

Adult↗

PubMed2001

Evidence for an association between polymorphism in the serotonin-2A receptor variant (102T/C) and increment of N100 amplitude in schizophrenics treated with clozapine.

Using event-related potentials (ERPs), a reduction in the auditory N100, N200 and P300 amplitude has been found in schizophrenic patients and may represent some pathophysiological deficit. Therefore, we investigated whether the genetic variant of the serotonin-2A receptor is associated with ERP change after clozapine treatment in schizophrenic patients. Ninety-nine schizophrenic patients were included in the study. The results demonstrated that patients with 102C/C genotype have higher N100 amplitude than other patients after clozapine treatment. Our findings suggested that serotonin-2A receptor polymorphism may relate to clozapine response in schizophrenic patients. An objective and reliable tool like ERPs to assess patients' treatment response may afford more consistent results in pharmacogenetic studies.

Adult↗

PubMed2001

Association study for a functional serotonin transporter gene polymorphism and late-onset Alzheimer's disease for Chinese patients.

Two recent studies have demonstrated an association for a deletion/insertion polymorphism within the promoter region of the serotonin transporter gene (5-HTTLPR), and Alzheimer's disease (AD). According to these studies, subjects with the short variant of the 5-HTTLPR gene are at increased risk for AD; however, this finding has not been confirmed by other workers. To evaluate the role of the 5-HTTLPR gene in susceptibility for AD, we conducted an association study for this polymorphism in a Chinese population. No significant differences were determined for genotype distribution or allele frequencies, comparing AD patients and normal controls. Even dividing the population into subgroups according to the presence of the APOE epsilon4 allele, no differences for genotype or allele frequencies were determined, comparing patients and controls. These results suggest that it is unlikely that the 5-HTTLPR polymorphism plays a substantial role in conferring susceptibility to AD.

Aged↗

PubMed2001

Association study of angiotensin-converting enzyme gene polymorphism with schizophrenia and polydipsia.

Angiotensin-converting enzyme (ACE) is a key enzyme in the renin-angiotensin system and can modulate dopamine turnover in the midbrain. Previous studies have revealed changes in the central ACE levels for schizophrenic patients, possibly related to the polydipsia commonly demonstrated for chronic schizophrenia. An insertion (I)/deletion (D) polymorphism of the ACE gene has been associated with ACE levels. Therefore, we elected to investigate the ACE I/D polymorphism for 124 schizophrenic patients and 117 control subjects. No significant differences for the genotype distribution or the allele frequency were revealed comparing controls and schizophrenic patients. The ACE genotypes were not associated with onset age or psychiatric symptoms for the schizophrenic cases. A modest association was revealed for this ACE polymorphism and polydipsia diagnosis for these patients. Using bearers of the D allele as baseline, the ratio for I/I homozygote was 2.31 (95% CI 0.95-5.65). This association needs further replication as it may have implications for the pathogenesis and the treatment of polydipsia for schizophrenic patients.

Adult↗

PubMed2001

Association between the Ser9Gly polymorphism of the dopamine D3 receptor gene and tardive dyskinesia in Chinese schizophrenic patients.

It has been suggested that dopamine D3 receptor (DRD3) may have important implications for antipsychotic-induced tardive dyskinesia (TD). Previous studies have demonstrated an association between a serine to glycine polymorphism in the first exon of the DRD3 gene and TD; however, the results have been inconsistent. Therefore, we have replicated these studies using a Chinese sample population. A total of 115 schizophrenic patients from chronic wards were assessed for TD severity using the Abnormal Involuntary Movements Scale (AIMS) and were subsequently genotyped for the DRD3 polymorphism. The mean AIMS score for patients carrying the heterozygote (DRD3(ser-gly)) was significantly greater than for those with the homozygotes (DRD3(ser-ser) and DRD3(gly-gly)). Our results are in line with a previous report, the results of which suggest that the presence of the DRD3(ser-gly) genotype may be a risk factor for the development of TD in patients treated with antipsychotics.

Adolescent↗

PubMed2001

Association analysis of a functional G protein beta3 subunit gene polymorphism (C825T) in mood disorders.

The guanine nucleotide-binding proteins (G proteins), heterotrimers consisting of alpha, beta and gamma subunits, convey signals initiated by the activation of many neurotransmitter receptors. Evidence for involvement of the G proteins in mood disorders relies on the effects of mood stabilizers and antidepressants on G protein function. In addition, abnormalities in the expression of G proteins have been demonstrated in mood disorder patients. Therefore, we tested the hypothesis that a functional polymorphism (C825T) in the G protein beta3 gene subunit (GNB3) confers susceptibility to mood disorders. A population-based association study was utilized, and GNB3 was genotyped for 144 mood disorder patients and 153 normal controls. The results reveal that it is not likely that the C825T polymorphism in the GNB3 gene subunit is involved in mood disorder pathogenesis. Further studies of the associations between other G protein subunits and mood disorder are needed to fully elaborate the involvement of this protein in mood disorders.

Adult↗

PubMed2001

Association study of the 5-HT(6) receptor polymorphism (C267T) and symptomatology and antidepressant response in major depressive disorders.

The serotonergic neurotransmitter system has been implicated in the pathogenesis of major depressive disorder (MDD). Of the 14 human serotonin (5-HT) receptors, the 5-HT(6) receptor may be a candidate for the study of MDD because of its relative abundance in certain limbic areas and its high affinity to several antidepressants. The present study tested the hypothesis that a 5-HT(6) genetic polymorphism (C267T) is associated with the clinical manifestations of, and/or antidepressant response in, MDD. The Hamilton Depression Rating Scale was used to assess 57 MDD patients before antidepressant treatment, with 34 patients completing the 4-week treatment and evaluation. The results of the association study provide that the 5-HT(6) C267T genetic variant does not play a major role in producing the clinical manifestations or antidepressant response for MDD patients. Further study with a functional 5-HT(6) polymorphism is needed to explore the role of 5-HT(6) in the pathogenesis of MDD.

Adult↗

PubMed2000

Intelligence and event-related potentials for young female human volunteer apolipoprotein E epsilon4 and non-epsilon4 carriers.

The apolipoprotein E (APOE) epsilon4 allele is associated with late-onset Alzheimer's disease and cognitive function in aging normal populations. To study the effect of the presence of the epsilon4 allele on cognitive function, we compared intelligence-test scores and component values for event-related potentials for epsilon4 and non-epsilon4 carriers in a group of 134 young females. The results demonstrate modest increases in performance intelligence quotient (IQ) and N100 amplitude for epsilon4 carriers (P=0.038 and 0.068, respectively). Our findings suggest that cognitive impairment, associated with the presence of the epsilon4 allele, is age-dependent and thus not probable for young women. The higher performance IQ scores demonstrated for epsilon4 carriers require further exploration.

Adult↗

PubMed2000

Association study of a functional serotonin transporter gene polymorphism with schizophrenia, psychopathology and clozapine response.

Serotonin is implicated in the pathogenesis of schizophrenia. Following serotonin release, the serotonin transporter (5-HTT) is the major determinant of serotonin inactivation. The present study tested the hypothesis that a biallelic polymorphism in the 5' regulatory region of the 5-HTT gene (5-HTTLPR) confers susceptibility to schizophrenia, association with the clinical manifestations of schizophrenia or clozapine response. 90 treatment-resistant schizophrenic patients were assessed using the Brief Psychiatric Rating Scale before and after clozapine treatment. The results demonstrated that the 5-HTTLPR variants did not play a major role in the susceptibility, clinical manifestations or clozapine response in schizophrenia.

Adult↗

PubMed2000

No association between butyrylcholinesterase K-variant and Alzheimer disease in Chinese.

Increased butyrylcholinesterase (BChE) activity has been reported to be associated with the formation of amyloid plaques and neurofibrillary tangles and may consequently be involved in the pathogenesis of Alzheimer disease (AD). Because the catalytic activity of BChE-K variant is reduced by one-third compared with non-variant, we speculated that BChE-K variant has a protective effect on AD. However, Lehmann et al. [1997] reported a synergistic effect between the genes for BChE-K variant and apolipoprotein E (ApoE) epsilon 4, which increases the risk for late onset AD. In the present study, we tested 89 Chinese AD patients and 101 Chinese controls and found no evidence of association between BCHE-K and AD of either early or late onset (age > 65 years). No evidence of a synergistic effect was found between the BCHE-K variant and APOE epsilon 4 in this study. Our data suggest that BChE-K variant has no modifying effect on the pathogenesis of AD. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:167-169, 2000.

Aged↗

PubMed2000

Association study of a cannabinoid receptor gene (CNR1) polymorphism and schizophrenia.

Cannabis can induce schizophrenic-like symptoms in healthy individuals. A principal active ingredient of cannabis, delta-9-tetrahydrocannabinol, acts in the brain on a specific receptor, termed the cannabinoid receptor 1 (CNR1). The human gene for CNR1 is mapped to chromosome 6q14-15, and linkage studies have produced evidence for a schizophrenia-susceptibility locus in this region. To explore a possible role for CNR1 in the pathogenesis of schizophrenic disorders, we used an association study to genotype the CNR1 polymorphism for 127 schizophrenic patients and 146 control subjects. The results demonstrate no association between CNR1 genotypes and schizophrenic disorders (P = 0.409), with these negative findings suggesting that, for Chinese populations, the (AAT)n triplet repeat in the promoter region of the CNR1 gene is not directly involved in the pathogenesis of schizophrenic disorders.

Adult↗

PubMed2000

No evidence for association of alpha 1a adrenoceptor gene polymorphism and clozapine-induced urinary incontinence.

Clozapine is an effective atypical antipsychotic that has high affinity for many neurotransmitter receptors. Among the adverse effects of clozapine, urinary incontinence is commonly found and is suggested to be caused by alpha-adrenergic blockade. We tested the hypothesis that clozapine-induced urinary incontinence is related to a genetic variant of the alpha(1a)-adrenoceptor. We also tested whether the alpha(1a)-receptor gene confers susceptibility to schizophrenic disorders. Our result indicated that the alpha(1a)-adrenoceptor gene polymorphism investigated plays no major role in the pathogenesis of schizophrenia or in clozapine-induced urinary incontinence. Considering the superior effects of clozapine and its potent adrenergic antagonistic effects, it is of interest to investigate the association between this polymorphism and the treatment response.

Adult↗

PubMed2000

Association study of apolipoprotein E epsilon4 with clinical phenotype and clozapine response in schizophrenia.

Schizophrenic patients with the apolipoprotein E (APOE = gene; apoE = protein) epsilon4 allele exhibited lower psychosis scores than patients without the epsilon4 allele in previous reports. The present study tested the hypothesis that the APOE epsilon4 allele confers association with the clinical manifestations of schizophrenia or clozapine response. A total of 95 schizophrenic patients who were treatment resistant were included in the study. The results demonstrated that the presence of the APOE epsilon4 allele did not influence the response to clozapine in schizophrenic patients, neither was the baseline psychopathology related to the APOE epsilon4 allele. Given the multiple functions of the apoE protein in the brain, further study of the influence of APOE on CNS medication response is needed.

Adult↗

PubMed1999

Tryptophan hydroxylase gene polymorphism (A218C) and suicidal behaviors.

Serotonergic dysfunction is implicated in mood disorders and suicidal behaviors. Genetic variants of tryptophan hydroxylase (TPH), a rate-limiting enzyme in the biosynthesis of serotonin, were associated with suicidal behaviors in three reports, but were not found in other studies. We investigated the TPH A218C polymorphism in 151 subjects with mood disorders and 200 control subjects. The results demonstrated a significant difference in genotypic distribution between controls and depressed patients, but not bipolar patients. A positive association between TPH polymorphism and suicidal behaviors was found in depressed patients and not in bipolar patients. We suggest that the association of TPH variants and suicide might depend on the diagnosis, and TPH mutation plays no major role in the pathogenesis of bipolar disorders.

Adult↗

PubMed1999

Association analysis of the 5-HT(6) receptor polymorphism (C267T) in mood disorders.

The serotonergic system is implicated in the etiology of mood disorders. Among those most recently discovered serotonin receptors, the relative abundance of serotonin type 6 receptor (5-HT(6)) in the limbic area and the high affinity of some antidepressants to 5-HT(6) receptors suggest that this receptor might be involved in the pathogenesis of mood disorders. In a population-based association study, we tested the hypothesis that the allelic variant (C267T) of the human 5-HT(6) gene confers susceptibility to mood disorders. We genotyped the 5-HT(6) receptor in 139 patients with mood disorders and 147 controls. The results demonstrated that there were no significant differences in genotype or allele frequencies between controls and all patients, or between controls and patients with bipolar disorders or major depression, separately. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 88:601-602, 1999.

Adult↗