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5HTR2A gene polymorphism and personality traits in patients with major psychoses.

https://arctichealth.org/en/permalink/ahliterature190821
Source
Eur Psychiatry. 2002 Mar;17(1):24-8
Publication Type
Article
Date
Mar-2002
Author
V E Golimbet
M V Alfimova
K K Manandyan
N G Mitushina
L I Abramova
V G Kaleda
I V Oleichik
YuB Yurov
V I Trubnikov
Author Affiliation
Laboratory of Preventive Genetics, Research Mental Health Center, Russian Academy of Medical Sciences, Zagorodnoe sh. 2/2, Moscow, Russia 113152. golimbet@mail.ru
Source
Eur Psychiatry. 2002 Mar;17(1):24-8
Date
Mar-2002
Language
English
Publication Type
Article
Keywords
Adult
Analysis of Variance
Female
Humans
Male
Moscow
Personality - genetics
Personality Inventory
Polymorphism, Genetic - genetics
Psychiatric Status Rating Scales
Psychotic Disorders - genetics
Receptors, Serotonin - genetics
Abstract
Serotonin receptor (5HTR2A) gene polymorphism has been reported to be associated with clinical phenotypes in schizophrenia. The current study attempted to investigate a relationship between 5HTR2A 102T/C polymorphism and personality traits as well as clinical symptoms in patients with ICD-10 diagnoses of schizophrenia and affective disorders. 5HTR2A genotyping, clinical and psychological assessment were administered to 375 patients, 104 first-degree healthy relatives of the patients and 157 controls. In the patients an association was observed between the 2/2 5HTR2A genotype and scores on the Hypochondriasis scale (MMPI) (ANOVA, F = 4.56; P = 0.011) and trait anxiety (F = 4.21; P = 0.002). A significant difference between 1/1 and 2/2 genotypes has been also found for Neuroticism scores (EPI) (t = 2.18; P = 0.0031). No significant differences by 5HTR2A genotype were observed in either the control or first-degree relatives group for all scales studied. Positive, negative and psychopathological symptoms emerged higher in the 2/2 genotype patients compared to other genotype carriers. Therefore, the 2/2 genotype may contribute to produce the phenotype, with specific clinical and pathological features in common, regardless of nosologic heterogeneity of psychoses.
PubMed ID
11918989 View in PubMed
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Differences and similarities in the serotonergic diathesis for suicide attempts and mood disorders: a 22-year longitudinal gene-environment study.

https://arctichealth.org/en/permalink/ahliterature151424
Source
Mol Psychiatry. 2010 Aug;15(8):831-43
Publication Type
Article
Date
Aug-2010
Author
J. Brezo
A. Bureau
C. Mérette
V. Jomphe
E D Barker
F. Vitaro
M. Hébert
R. Carbonneau
R E Tremblay
G. Turecki
Author Affiliation
The McGill Group for Suicide Studies, Douglas Hospital Research Centre, McGill University, Montreal, QC, Canada.
Source
Mol Psychiatry. 2010 Aug;15(8):831-43
Date
Aug-2010
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Analysis of Variance
Child
Child Abuse, Sexual - psychology
Disease Susceptibility
Environment
Epistasis, Genetic
Family - psychology
Female
Humans
Longitudinal Studies
Male
Models, Biological
Mood Disorders - epidemiology - genetics - psychology
Odds Ratio
Polymorphism, Single Nucleotide
Probability
Quebec - epidemiology
Receptors, Serotonin - genetics
Risk factors
Serotonin - genetics - metabolism
Serotonin Plasma Membrane Transport Proteins - genetics
Suicide, Attempted - psychology
Tryptophan Hydroxylase - genetics
Young Adult
Abstract
To investigate similarities and differences in the serotonergic diathesis for mood disorders and suicide attempts, we conducted a study in a cohort followed longitudinally for 22 years. A total of 1255 members of this cohort, which is representative of the French-speaking population of Quebec, were investigated. Main outcome measures included (1) mood disorders (bipolar disorder and major depression) and suicide attempts by early adulthood; (2) odds ratios and probabilities associated with 143 single nucleotide polymorphisms in 11 serotonergic genes, acting directly or as moderators in gene-environment interactions with childhood sexual or childhood physical abuse (CPA), and in gene-gene interactions; (3) regression coefficients for putative endophenotypes for mood disorders (childhood anxiousness) and suicide attempts (childhood disruptiveness). Five genes showed significant adjusted effects (HTR2A, TPH1, HTR5A, SLC6A4 and HTR1A). Of these, HTR2A variation influenced both suicide attempts and mood disorders, although through different mechanisms. In suicide attempts, HTR2A variants (rs6561333, rs7997012 and rs1885884) were involved through interactions with histories of sexual and physical abuse whereas in mood disorders through one main effect (rs9316235). In terms of phenotype-specific contributions, TPH1 variation (rs10488683) was relevant only in the diathesis for suicide attempts. Three genes contributed exclusively to mood disorders, one through a main effect (HTR5A (rs1657268)) and two through gene-environment interactions with CPA (HTR1A (rs878567) and SLC6A4 (rs3794808)). Childhood anxiousness did not mediate the effects of HTR2A and HTR5A on mood disorders, nor did childhood disruptiveness mediate the effects of TPH1 on suicide attempts. Of the serotonergic genes implicated in mood disorders and suicidal behaviors, four exhibited phenotype-specific effects, suggesting that despite their high concordance and common genetic determinants, suicide attempts and mood disorders may also have partially independent etiological pathways. To identify where these pathways diverge, we need to understand the differential, phenotype-specific gene-environment interactions such as the ones observed in the present study, using suitably powered samples.
PubMed ID
19381154 View in PubMed
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A dominant gene for developmental dyslexia on chromosome 3.

https://arctichealth.org/en/permalink/ahliterature193082
Source
J Med Genet. 2001 Oct;38(10):658-64
Publication Type
Article
Date
Oct-2001
Author
J. Nopola-Hemmi
B. Myllyluoma
T. Haltia
M. Taipale
V. Ollikainen
T. Ahonen
A. Voutilainen
J. Kere
E. Widén
Author Affiliation
Department of Paediatric Neurology, Hospital for Children and Adolescents, University of Helsinki, Finland.
Source
J Med Genet. 2001 Oct;38(10):658-64
Date
Oct-2001
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Analysis of Variance
Child
Chromosome Mapping
Chromosomes, Human, Pair 3 - genetics
Dyslexia - genetics - physiopathology
Female
Finland
Genes, Dominant - genetics
Haplotypes - genetics
Humans
Lod Score
Male
Memory - physiology
Middle Aged
Pedigree
Psychological Tests
Radiation Hybrid Mapping
Reading
Receptors, Dopamine D2 - genetics
Receptors, Dopamine D3
Receptors, Serotonin - genetics
Abstract
Developmental dyslexia is a neurofunctional disorder characterised by an unexpected difficulty in learning to read and write despite adequate intelligence, motivation, and education. Previous studies have suggested mostly quantitative susceptibility loci for dyslexia on chromosomes 1, 2, 6, and 15, but no genes have been identified yet. We studied a large pedigree, ascertained from 140 families considered, segregating pronounced dyslexia in an autosomal dominant fashion. Affected status and the subtype of dyslexia were determined by neuropsychological tests. A genome scan with 320 markers showed a novel dominant locus linked to dyslexia in the pericentromeric region of chromosome 3 with a multipoint lod score of 3.84. Nineteen out of 21 affected pedigree members shared this region identical by descent (corrected p
Notes
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PubMed ID
11584043 View in PubMed
Less detail

Genetic linkage analysis of manic depression in Iceland.

https://arctichealth.org/en/permalink/ahliterature46569
Source
J R Soc Med. 1993 Sep;86(9):506-10
Publication Type
Article
Date
Sep-1993
Author
D. Curtis
R. Sherrington
P. Brett
D S Holmes
G. Kalsi
J. Brynjolfsson
H. Petursson
L. Rifkin
P. Murphy
E. Moloney
Author Affiliation
Academic Department of Psychiatry, St Mary's Hospital Medical School, London, UK.
Source
J R Soc Med. 1993 Sep;86(9):506-10
Date
Sep-1993
Language
English
Publication Type
Article
Keywords
Algorithms
Bipolar Disorder - genetics
Computer simulation
Dopamine beta-Hydroxylase - genetics
Enkephalins - genetics
Female
Humans
Iceland
Linkage (Genetics)
Male
Pedigree
Protein Precursors - genetics
Receptors, Serotonin - genetics
Research Support, Non-U.S. Gov't
Tyrosine 3-Monooxygenase - genetics
Abstract
Genetic linkage analysis has been used to study five Icelandic pedigrees multiply affected with manic depression. Genetic markers were chosen from regions which had been implicated by other studies or to which candidate genes had been localized. The transmission model used was of a dominant gene with incomplete penetrance and allowing for a large number of phenocopies, especially for unipolar rather than bipolar cases. Multipoint analysis with linked markers enabled information to be gained from regions spanning large distances. Using this approach we have excluded regions of chromosome 11p, 11q, 8q, 5q, 9q and Xq. Candidate genes excluded include those for tyrosine hydroxylase, the dopamine type 2 receptor, proenkephalin, the 5HT1A receptor and dopamine beta hydroxylase. Nevertheless, we remain optimistic that this approach will eventually identify at least some of the genes predisposing to manic depression.
PubMed ID
8105081 View in PubMed
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HTR3B is associated with alcoholism with antisocial behavior and alpha EEG power--an intermediate phenotype for alcoholism and co-morbid behaviors.

https://arctichealth.org/en/permalink/ahliterature152847
Source
Alcohol. 2009 Feb;43(1):73-84
Publication Type
Article
Date
Feb-2009
Author
Francesca Ducci
Mary-Anne Enoch
Qiaoping Yuan
Pei-Hong Shen
Kenneth V White
Colin Hodgkinson
Bernard Albaugh
Matti Virkkunen
David Goldman
Author Affiliation
Division of Psychological SGDP Centre, P080 Institue of Psychiatry 16 De Crespigny Park, London SE58AF, United Kingdom. Francesca.Ducci@iop.kcl.uk
Source
Alcohol. 2009 Feb;43(1):73-84
Date
Feb-2009
Language
English
Publication Type
Article
Keywords
Adult
African Americans
Alcoholism - complications - genetics - psychology
Alleles
Alpha Rhythm
Antisocial Personality Disorder - complications - genetics - psychology
Case-Control Studies
Electroencephalography
European Continental Ancestry Group
Female
Finland - epidemiology
Gene Frequency
Haplotypes
Humans
Indians, North American
Male
Mental Disorders - genetics - psychology
Phenotype
Polymorphism, Single Nucleotide
Psychiatric Status Rating Scales
Receptors, Serotonin - genetics
Receptors, Serotonin, 5-HT3
Risk factors
Young Adult
Abstract
Alcohol use disorders (AUD) with co-morbid antisocial personality disorder (ASPD) have been associated with serotonin (5-HT) dysfunction. 5-HT3 receptors are potentiated by ethanol and appear to modulate reward. 5-HT3 receptor antagonists may be useful in the treatment of early-onset alcoholics with co-morbid ASPD. Low-voltage alpha electroencephalogram (EEG) power, a highly heritable trait, has been associated with both AUD and ASPD. A recent whole genome linkage scan in one of our samples, Plains American Indians (PI), has shown a suggestive linkage peak for alpha power at the 5-HT3R locus. We tested whether genetic variation within the HTR3A and HTR3B genes influences vulnerability to AUD with comorbid ASPD (AUD+ASPD) and moderates alpha power. Our study included three samples: 284 criminal alcoholic Finnish Caucasians and 234 controls; two independent community-ascertained samples with resting EEG recordings: a predominantly Caucasian sample of 191 individuals (Bethesda) and 306 PI. In the Finns, an intronic HTR3B SNP rs3782025 was associated with AUD+ASPD (P=.004). In the Bethesda sample, the same allele predicted lower alpha power (P=7.37e(-5)). Associations between alpha power and two other HTR3B SNPs were also observed among PI (P=.03). One haplotype in the haplotype block at the 3' region of the gene that included rs3782025 was associated with AUD+ASPD in the Finns (P=.02) and with reduced alpha power in the Bethesda population (P=.00009). Another haplotype in this block was associated with alpha power among PI (P=.03). No associations were found for HTR3A. Genetic variation within HTR3B may influence vulnerability to develop AUD with comorbid ASPD. 5-HT3R might contribute to the imbalance between excitation and inhibition that characterize the brain of alcoholics.
Notes
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PubMed ID
19185213 View in PubMed
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Impaired repression at a 5-hydroxytryptamine 1A receptor gene polymorphism associated with major depression and suicide.

https://arctichealth.org/en/permalink/ahliterature183572
Source
J Neurosci. 2003 Sep 24;23(25):8788-99
Publication Type
Article
Date
Sep-24-2003
Author
Sylvie Lemonde
Gustavo Turecki
David Bakish
Lisheng Du
Pavel D Hrdina
Christopher D Bown
Adolfo Sequeira
Neena Kushwaha
Stephen J Morris
Ajoy Basak
Xiao-Ming Ou
Paul R Albert
Author Affiliation
Ottawa Health Research Institute (Neuroscience), University of Ottawa, Department of Medicine, Ottawa, Canada, K1H 8M5.
Source
J Neurosci. 2003 Sep 24;23(25):8788-99
Date
Sep-24-2003
Language
English
Publication Type
Article
Keywords
Adult
Animals
Clone Cells
DNA - metabolism
Depressive Disorder, Major - epidemiology - genetics
Down-Regulation - genetics
Drosophila Proteins
European Continental Ancestry Group - genetics
Female
Genetic Linkage
Genetic Predisposition to Disease
Genetic Testing
Humans
Macromolecular Substances
Male
Nuclear Proteins - metabolism
Ontario - epidemiology
Polymorphism, Genetic - genetics
Promoter Regions, Genetic - physiology
Protein Binding - physiology
Protein Structure, Tertiary - physiology
Raphe Nuclei - chemistry - cytology - metabolism
Rats
Rats, Sprague-Dawley
Receptors, Serotonin - genetics
Receptors, Serotonin, 5-HT1
Repressor Proteins - metabolism
Suicide - statistics & numerical data
Transfection
Abstract
Inhibition of serotonergic raphe neurons is mediated by somatodendritic 5-HT1A autoreceptors, which may be increased in depressed patients. We report an association of the C(-1019)G 5-HT1A promoter polymorphism with major depression and suicide in separate cohorts. In depressed patients, the homozygous G(-1019) allele was enriched twofold versus controls (p = 0.0017 and 0.0006 for G/G genotype and G allele distribution, respectively), and in completed suicide cases the G(-1019) allele was enriched fourfold (p = 0.002 and 0.00008 for G/G genotype and G allele distribution, respectively). The C(-1019) allele was part of a 26 bp imperfect palindrome that bound transcription factors nuclear NUDR [nuclear deformed epidermal autoregulatory factor (DEAF-1)]/suppressin and Hairy/Enhancer-of-split-5 (Drosophila) (Hes5) to repress 5-HT1A or heterologous promoters, whereas the G(-1019) allele abolished repression by NUDR, but only partially impaired Hes5-mediated repression. Recombinant NUDR bound specifically to the 26 bp palindrome, and endogenous NUDR was present in the major protein-DNA complex from raphe nuclear extracts. Stable expression of NUDR in raphe cells reduced levels of endogenous 5-HT1A protein and binding. NUDR protein was colocalized with 5-HT1A receptors in serotonergic raphe cells, hippocampal and cortical neurons, and adult brain regions including raphe nuclei, indicating a role in regulating 5-HT1A autoreceptor expression. Our data indicate that NUDR is a repressor of the 5-HT1A receptor in raphe cells the function of which is abrogated by a promoter polymorphism. We suggest a novel transcriptional model in which the G(-1019) allele derepresses 5-HT1A autoreceptor expression to reduce serotonergic neurotransmission, predisposing to depression and suicide.
PubMed ID
14507979 View in PubMed
Less detail

Linkage of antisocial alcoholism to the serotonin 5-HT1B receptor gene in 2 populations.

https://arctichealth.org/en/permalink/ahliterature203917
Source
Arch Gen Psychiatry. 1998 Nov;55(11):989-94
Publication Type
Article
Date
Nov-1998
Author
J. Lappalainen
J C Long
M. Eggert
N. Ozaki
R W Robin
G L Brown
H. Naukkarinen
M. Virkkunen
M. Linnoila
D. Goldman
Author Affiliation
Section of Population Genetics and Linkage, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20852, USA.
Source
Arch Gen Psychiatry. 1998 Nov;55(11):989-94
Date
Nov-1998
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Alcoholism - epidemiology - genetics
Animals
Antisocial Personality Disorder - epidemiology - genetics
Base Sequence
Comorbidity
Female
Finland - epidemiology - ethnology
Genetic Linkage
Genotype
Humans
Impulse Control Disorders - epidemiology - genetics
Indians, North American - genetics
Male
Mice
Molecular Sequence Data
Pedigree
Polymorphism, Genetic
Receptor, Serotonin, 5-HT1B
Receptors, Serotonin - genetics
Southwestern United States - epidemiology
Tandem Repeat Sequences - genetics
Abstract
In mice, quantitative trait locus studies and behavioral evaluation of animals deleted for 5-HT1B have implicated this serotonin autoreceptor in alcohol consumption and aggressive behavior. We therefore investigated whether the 5-HT1B gene (HTR1B) is linked to alcoholism with aggressive and impulsive behavior in the human, as represented by 2 psychiatric diagnoses: antisocial personality disorder and intermittent explosive disorder comorbid with alcoholism.
Linkage was first tested in 640 Finnish subjects, including 166 alcoholic criminal offenders, 261 relatives, and 213 healthy controls. This was followed by a study in a large multigenerational family derived from a Southwestern American Indian tribe (n=418) with a high rate of alcoholism. All subjects were psychiatrically interviewed, blind-rated for psychiatric diagnoses, and typed for a HTR1B G861C polymorphism and for a closely linked short-tandem repeat locus, D6S284. Linkage was evaluated in sib pairs, and by using an association approach in which pedigree randomization corrects for nonindependence of observations on related subjects.
In Finnish sib pairs, antisocial alcoholism showed significant evidence of linkage to HTR1B G861C (P=.04) and weak evidence with D6S284 (P=.06). By association analysis, the 183 Finnish antisocial alcoholics had a significantly higher HTR1B-861C allele frequency than the other 457 Finns we studied (P=.005). In the Southwestern American Indian tribe, significant sib pair linkage of antisocial alcoholism to HTR1B G861C (P=.01) was again observed, and there was also significant linkage to D6S284 (P=.01).
These results suggest that a locus predisposing to antisocial alcoholism may be linked to HTR1B at 6q13-15.
PubMed ID
9819067 View in PubMed
Less detail

Mutation screening of the 5-hydroxytryptamine7 receptor gene among Finnish alcoholics and controls.

https://arctichealth.org/en/permalink/ahliterature204805
Source
Psychiatry Res. 1998 Feb 27;77(3):139-45
Publication Type
Article
Date
Feb-27-1998
Author
U. Pesonen
M. Koulu
A. Bergen
M. Eggert
H. Naukkarinen
M. Virkkunen
M. Linnoila
D. Goldman
Author Affiliation
Department of Pharmacology and Clinical Pharmacology, MediCity Research Laboratory, University of Turku, Finland. upeso@utu.fi
Source
Psychiatry Res. 1998 Feb 27;77(3):139-45
Date
Feb-27-1998
Language
English
Publication Type
Article
Keywords
Adult
Alcoholism - genetics
Alleles
Amino Acid Substitution - genetics
DNA Mutational Analysis
Female
Finland
Gene Frequency - genetics
Genetic Testing
Genotype
Humans
Male
Middle Aged
Point Mutation - genetics
Polymorphism, Genetic
Receptors, Serotonin - genetics
Abstract
Impaired central serotonin neurotransmission has been associated with increased aggression, impaired impulse control and diurnal activity rhythm disturbances among humans. Neuroanatomic distribution and pharmacological properties of the serotonin 5-HT7 receptor suggest that it may play a role in psychiatric disorders and in circadian rhythm regulation. In this study a point mutation causing proline279 --> leucine amino acid substitution in the 5-hydroxytryptamine7 (5-HT7) receptor gene was discovered. This 5-HT7Leu279 variant was observed in six of 825 individuals, all of whom are heterozygous for the substitution. Three of them are alcoholic offenders (3/255), two are relatives of an offender without the 5-HT7Leu279 allele (2/255) and one is a healthy control without any psychiatric diagnosis (1/248). The allele frequency of the 5-HT7Leu279 variant is 0.004 (6/758) among Finns. Although the 5-HT7Leu279 variant is approximately three times more common among alcoholic offenders than among healthy controls, it is not significantly associated with alcoholism or impulsivity in the present study. The 5-HT7Leu279 allele may, however, be a predisposing allele in a subgroup of alcoholic offenders with multiple behavioral problems.
PubMed ID
9707296 View in PubMed
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[Polymorphism of the serotonin receptor (5-HTR2A) gene and verbal fluency in normalcy and schizophrenia].

https://arctichealth.org/en/permalink/ahliterature186348
Source
Mol Biol (Mosk). 2003 Jan-Feb;37(1):68-73
Publication Type
Article
Author
M V Alfimova
V E Golimbet
N G Mitiushina
Author Affiliation
Mental Health Research Center, Russian Academy of Medical Sciences, Moscow, 113152 Russia.
Source
Mol Biol (Mosk). 2003 Jan-Feb;37(1):68-73
Language
Russian
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Female
Humans
Male
Middle Aged
Moscow
Polymorphism, Genetic
Receptor, Serotonin, 5-HT2A
Receptors, Serotonin - genetics
Reference Values
Schizophrenia - complications - genetics - physiopathology
Speech - physiology
Speech Disorders - complications - diagnosis - genetics
Abstract
To study the effect of the serotonergic brain system on verbal fluency (i.e., the ability to rapidly extract necessary words from the vocabulary), the T102C polymorphism of the serotonin receptor type 2A (5-HTR2A) gene was tested for association with verbal fluency in 108 patients with schizophrenia or schizotypic disorders and 97 mentally healthy individuals. A significant association was observed only in male schizophrenics (N = 67), with homozygotes A2A2 having lower verbal fluency. The results did not support the association between the 5-HTR2A polymorphism and verbal fluency in normalcy, and agree with the assumed contribution of genotype A2A2 to the severity of schizophrenia.
PubMed ID
12624948 View in PubMed
Less detail

Schizophrenia and the serotonin transporter gene.

https://arctichealth.org/en/permalink/ahliterature203579
Source
Psychiatr Genet. 1998;8(4):207-12
Publication Type
Article
Date
1998
Author
D. Rao
E G Jönsson
S. Paus
R. Ganguli
M. Nöthen
V L Nimgaonkar
Author Affiliation
Department of Psychiatry, University of Pittsburgh School of Medicine, Western Psychiatric Institute and Clinic, PA 15213, USA.
Source
Psychiatr Genet. 1998;8(4):207-12
Date
1998
Language
English
Publication Type
Article
Keywords
Adult
African Continental Ancestry Group - genetics
Age of Onset
Alleles
Antipsychotic Agents - therapeutic use
Carrier Proteins - genetics
Case-Control Studies
Cohort Studies
European Continental Ancestry Group - genetics
Genetic Predisposition to Disease
Humans
Life tables
Membrane Glycoproteins - genetics
Membrane Transport Proteins
Middle Aged
Nerve Tissue Proteins
Pennsylvania - epidemiology
Polymorphism, Genetic
Promoter Regions, Genetic - genetics
Receptor, Serotonin, 5-HT2A
Receptors, Serotonin - genetics
Risk factors
Schizophrenia - epidemiology - genetics
Serotonin Plasma Membrane Transport Proteins
Survival Analysis
Sweden - epidemiology
Treatment Outcome
Abstract
A case control study was conducted among cases with schizophrenia (DSM IV criteria) and screened adult controls from three cohorts. Bi-allelic polymorphisms in the promoter region of the serotonin transporter gene (5-HTT) were examined in conjunction with those of the serotonin 5-HT2a receptor (HTR2). No significant association with 5-HTT was detected among US Caucasians (n = 207), African-Americans (n = 84) or Caucasians from Sweden (n = 221). However, survival analysis suggested an association with the age at onset among the Swedish cases. The association should be considered tentative as it was not evident in the smaller US samples. The following exploratory analyses among the US samples were also not significant: associations with subgroups of patients based on familiality or response to medications, or altered risk due to the joint effects of 5-HTT and HTR2 genotypes.
Notes
Erratum In: Psychiatr Genet 1999 Mar;9(1):51
PubMed ID
9861638 View in PubMed
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