No Association Between Catecholamine-O-Methyltransferase Gene Polymorphism and Bipolar Disorder and it Subtypes

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
A. Leszczyńska-Rodziewicz ◽  
M. Dmitrzak-Weglarz ◽  
M. Skibinska ◽  
J. Rybakowski ◽  
J. Hauser

Aims:The catecholamine hypothesis of affective disorders suggests that depression is associated with a functional decrease of catecholamines. There is consistent evidence that COMT gene would be a candidate gene for studies of bipolar disorder.Methods:The study was performed on patients with bipolar disorder n=298 (male n=126, female n=172). Control subjects were blood donors n=336 (male n=130, female n=206), who were not psychiatrically assessed. The subgroup of patients with psychotic features not congruent with mood contained n=88 patients, males n=41, females n=47. The subgroup of patients with psychotic features congruent with mood contained n=89 patients, males n=47, females n=42. The subgroup of patients with melancholic depression contained n=197 patients, males n=76, females n= 121. A polymorphism was analysed by PCR-RFLP method.Results:There were no differences in the frequency of genotypes, alleles between patients and controls in the whole group (p=0,286 for genotypes, p= 0,652 for alleles). Dividing the patients according to the gender, no differences in the frequency of either genotypes or alleles were found (p=0,298 for genotype males, p=0,456 for genotypes females). We did not find the association in the subgroup of patients with psychotic features congruent (p=0,828 for genotypes, p= 0,866 for alleles), or not congruent with mood (p=0,116 for genotypes, p= 0,673 for alleles) and with the subgroup of patients with depression with melancholic features (p= 0,758 for genotypes, p= 0,849 for alleles).Conclusion:Results of our study suggest that the polymorphism of COMT gene is not associated with the susceptibility to bipolar disorder.

2002 ◽  
Vol 51 (9) ◽  
pp. 762-765 ◽  
Author(s):  
Béatrice Bonnier ◽  
Philip Gorwood ◽  
Michel Hamon ◽  
Yves Sarfati ◽  
Claudette Boni ◽  
...  

2020 ◽  
pp. 1-11 ◽  
Author(s):  
Igor Nenadić ◽  
Tina Meller ◽  
Simon Schmitt ◽  
Frederike Stein ◽  
Katharina Brosch ◽  
...  

Abstract Background Schizotypy is a putative risk phenotype for psychosis liability, but the overlap of its genetic architecture with schizophrenia is poorly understood. Methods We tested the hypothesis that dimensions of schizotypy (assessed with the SPQ-B) are associated with a polygenic risk score (PRS) for schizophrenia in a sample of 623 psychiatrically healthy, non-clinical subjects from the FOR2107 multi-centre study and a second sample of 1133 blood donors. Results We did not find correlations of schizophrenia PRS with either overall SPQ or specific dimension scores, nor with adjusted schizotypy scores derived from the SPQ (addressing inter-scale variance). Also, PRS for affective disorders (bipolar disorder and major depression) were not significantly associated with schizotypy. Conclusions This important negative finding demonstrates that despite the hypothesised continuum of schizotypy and schizophrenia, schizotypy might share less genetic risk with schizophrenia than previously assumed (and possibly less compared to psychotic-like experiences).


Author(s):  
Anna Leszczyńska-Rodziewicz ◽  
Aleksandra Szczepankiewicz ◽  
Maria Skibińska ◽  
Joanna Pawlak ◽  
Monika Dmitrzak-Węglarz ◽  
...  

2020 ◽  
Vol 63 (6) ◽  
pp. 40-50
Author(s):  
Hugo Enrique Hernández-Martínez ◽  
Marta Georgina Ochoa-Madrigal

The diagnosis and treatment of bipolar disorders (BPD) in children is currently one of the biggest challenges and area of controversy in the field of child psychiatry. Bipolar disorders encompass several affective disorders that involve alterations in the degree of activity, content and form of thinking that are characterized by biphasic episodes of mood. This group of disorders affect approximately 1% of the world population and begin in youth (the average age of onset of ~20 years). However, in some studies a delay of 5 years has been observed since the presentation of symptoms at the beginning of the treatment. Currently, the diagnosis of TBP in children and adolescents should be based on the same set of symptoms applied to adults, as well as the general principles of the treatment. The research carried out around this disorder has resulted in changes in the conceptualization and approach of this pathology, now conceived as a group of disorders that share changes in mood and other cardinal symptoms, of a chronic and progressive nature that impacts in a negative way in those who suffer them. Key words: Bipolar disorder; childhood; mania; hypomania; depression.


2001 ◽  
Vol 178 (S41) ◽  
pp. s128-s133 ◽  
Author(s):  
Nick Craddock ◽  
Ian Jones

BackgroundA robust body of evidence from family, twin and adoption studies demonstrates the importance of genes in the pathogenesis of bipolar disorder. Recent advances in molecular genetics have made it possible to identify these susceptibility genes.AimsTo present an overview for clinical psychiatrists.MethodReview of current molecular genetics approaches and emerging findings.ResultsOccasional families may exist in which a single gene plays a major role in determining susceptibility, but the majority of bipolar disorder involves more complex genetic mechanisms such as the interaction of multiple genes and environmental factors. Molecular genetic positional and candidate gene approaches are being used for the genetic dissection of bipolar disorder. No gene has yet been identified but promising findings are emerging. Regions of interest include chromosomes 4p16, 12q23–q24, 16p13, 21q22, and Xq24–q26. Candidate gene association studies are in progress but no robust positive findings have yet emerged.ConclusionIt is almost certain that over the next few years the identification of bipolar susceptiblity genes will have a major impact on our understanding of disease pathophysiology. This is likely to lead to major improvements and treatment in patient care, but will also raise important ethical issues.


2006 ◽  
Vol 18 (5) ◽  
pp. 193-209 ◽  
Author(s):  
Richard J. Porter ◽  
Peter Gallagher

Background:New evidence is emerging regarding abnormalities of hypothalamic-pituitary-adrenal (HPA) axis function in subtypes of affective disorders. Adverse effects of HPA axis dysregulation may include dysfunction of monoaminergic transmitter systems, cognitive impairment and peripheral effects. Newer treatments specifically targeting the HPA axis are being developed.Objective:To review these developments focusing particularly on the glucocorticoid receptor (GR) antagonist mifepristone.Method:A selective review of the literature.Results:The function of GRs is increasingly being defined. The role of corticotrophin-releasing hormone (CRH) and dehydroepiandrosterone (DHEA) in the brain is also increasingly understood. HPA axis function is particularly likely to be abnormal in psychotic depression and bipolar disorder, and it is in these conditions that trials of the GR antagonist mifepristone are being focused. CRH antagonists and DHEA are also being investigated as potential treatments.Conclusion:Initial studies of mifepristone and other HPA-axis-targeting agents in psychotic depression and bipolar disorder are encouraging and confirmatory studies are awaited.


CNS Spectrums ◽  
2003 ◽  
Vol 8 (2) ◽  
pp. 120-126 ◽  
Author(s):  
Alan B. Douglass

AbstractDoes narcolepsy, a neurological disease, need to be considered when diagnosing major mental illness? Clinicians have reported cases of narcolepsy with prominent hypnagogic hallucinations that were mistakenly diagnosed as schizophrenia. In some bipolar disorder patients with narcolepsy, the HH resulted in their receiving a more severe diagnosis (ie, bipolar disorder with psychotic features or schizoaffective disorder). The role of narcolepsy in psychiatric patients has remained obscure and problematic, and it may be more prevalent than commonly believed. Classical narcolepsy patients display the clinical “tetrad”—cataplexy, hypnagogic hallucinations, daytime sleep attacks, and sleep paralysis. Over 85% also display the human leukocyte antigen marker DQB10602 (subset of DQ6). Since 1998, discoveries in neuroanatomy and neurophysiology have greatly advanced the understanding of narcolepsy, which involves a nearly total loss of the recently discovered orexin/hypocretin (hypocretin) neurons of the hypothalamus, likely by an autoimmune mechanism. Hypocretin neurons normally supply excitatory signals to brainstem nuclei producing norepinephrine, serotonin, histamine, and dopamine, with resultant suppression of sleep. They also project to basal forebrain areas and cortex. A literature review regarding the differential diagnosis of narcolepsy, affective disorder, and schizophrenia is presented. Furthermore, it is now possible to rule out classical narcolepsy in difficult psychiatric cases. Surprisingly, psychotic patients with narcolepsy will likely require stimulants to fully recover. Many conventional antipsychotic drugs would worsen their symptoms and make them appear to become a “chronic psychotic,” while in fact they can now be properly diagnosed and treated.


2001 ◽  
Vol 33 (4) ◽  
pp. 248-256 ◽  
Author(s):  
Ian Jones ◽  
Nick Craddock

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