Parent of origin effect and allelic expression imbalance of the serotonin transporter in bipolar disorder and suicidal behaviour

Pinto, Crystal; Souza, Renan P.; Lioult, Diane; Semeralul, Mawahib O.; Kennedy, James L.; Warsh, Jerry J.; Wong, Albert H.C.; Luca, Vincenzo De

doi:10.1007/s00406-011-0192-8

Cited by 18 publications

(11 citation statements)

References 19 publications

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“…Altamura et al (2010), Baumann et al (1999), Bellivier et al (2000), Benedetti et al (2011), Berrettini et al (1986), Campos et al (2010), D’Ambrosio et al (2012), De Luca et al (2005a, 2005b, 2006, 2009), Dowlatshahi et al (1999), Dracheva et al (2008), Evans et al (2012), Feldcamp et al (2008), Finseth et al (2014), Jimenez et al (2013), Kamali et al (2012), Kim et al (2002, 2007, 2008), Le-Niculescu et al (2013), Leszczynska-Rodziewicz et al (2014), Lopez et al (2007), Mahon et al (2012), Malloy-Diniz et al (2011), Matsuo et al (2010), Monfrim et al (2014), Nery et al (2014), Nery-Fernandes et al (2012), Neves et al (2008, 2010), Park et al (2013), Perlis et al (2012), Pinto et al (2011), Pompili et al (2008), Shabani et al (2013), Sher et al (2006, 2012), Singhal et al (2014), Souery et al (2001), Stange et al (2014), Suttajit et al (2013), Thibodeau et al (2013), Tidemalm et al (2014), Tochigi et al (2008), Tsai et al (1999a), Vuksan-Cusa et al (2009) and Willour et al (2012).…”

Section: Figurementioning

confidence: 99%

Epidemiology, neurobiology and pharmacological interventions related to suicide deaths and suicide attempts in bipolar disorder: Part I of a report of the International Society for Bipolar Disorders Task Force on Suicide in Bipolar Disorder

Schaffer

Isometsä

Tondo

et al. 2015

Aust N Z J Psychiatry

140

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Objectives Bipolar disorder is associated with elevated risk of suicide attempts and deaths. Key aims of the International Society for Bipolar Disorders Task Force on Suicide included examining the extant literature on epidemiology, neurobiology and pharmacotherapy related to suicide attempts and deaths in bipolar disorder. Methods Systematic review of studies from 1 January 1980 to 30 May 2014 examining suicide attempts or deaths in bipolar disorder, with a specific focus on the incidence and characterization of suicide attempts and deaths, genetic and non-genetic biological studies and pharmacotherapy studies specific to bipolar disorder. We conducted pooled, weighted analyses of suicide rates. Results The pooled suicide rate in bipolar disorder is 164 per 100,000 person-years (95% confidence interval = [5, 324]). Sex-specific data on suicide rates identified a 1.7:1 ratio in men compared to women. People with bipolar disorder account for 3.4–14% of all suicide deaths, with self-poisoning and hanging being the most common methods. Epidemiological studies report that 23–26% of people with bipolar disorder attempt suicide, with higher rates in clinical samples. There are numerous genetic associations with suicide attempts and deaths in bipolar disorder, but few replication studies. Data on treatment with lithium or anticonvulsants are strongly suggestive for prevention of suicide attempts and deaths, but additional data are required before relative anti-suicide effects can be confirmed. There were limited data on potential anti-suicide effects of treatment with antipsychotics or antidepressants. Conclusion This analysis identified a lower estimated suicide rate in bipolar disorder than what was previously published. Understanding the overall risk of suicide deaths and attempts, and the most common methods, are important building blocks to greater awareness and improved interventions for suicide prevention in bipolar disorder. Replication of genetic findings and stronger prospective data on treatment options are required before more decisive conclusions can be made regarding the neurobiology and specific treatment of suicide risk in bipolar disorder.

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Section: Figurementioning

confidence: 99%

Epidemiology, neurobiology and pharmacological interventions related to suicide deaths and suicide attempts in bipolar disorder: Part I of a report of the International Society for Bipolar Disorders Task Force on Suicide in Bipolar Disorder

Schaffer

Isometsä

Tondo

et al. 2015

Aust N Z J Psychiatry

140

View full text Add to dashboard Cite

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“…Mendlewicz et al (2004) found no association for the 5-HTTLPR polymorphism with age-of-onset in BD or with BD in general ( N =572 BD cases). By contrast, Pinto et al (2011) did find a significant association between an earlier age of onset and the Short allele of the 5-HTTLPR polymorphism ( p =.02) in 350 BD patients and 693 unaffected relatives. Manchia et al (2010) and Mohammadi et al (2015) also found an association for earlier-onset and the Short allele of the 5-HTTLPR polymorphism in 230 and 150 BD patients, respectively.…”

Section: Candidate Gene-association Studiesmentioning

confidence: 66%

The genetics of early-onset bipolar disorder: A systematic review

Kennedy

Cullen

DeYoung

et al. 2015

Journal of Affective Disorders

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Background Early-onset bipolar disorder has been associated with a significantly worse prognosis than late-onset BD and has been hypothesized to be a genetically homogenous subset of BD. A sizeable number of studies have investigated early-onset BD through linkage-analyses, candidate-gene association studies, genome-wide association studies (GWAS), and analyses of copy number variants (CNVs), but this literature has not yet been reviewed. Methods A systematic review was conducted using the PubMed database on articles published online before January 15, 2015 and after 1990. Separate searches were made for linkage studies, candidate gene-association studies, GWAS, and studies on CNVs. Results Seventy-three studies were included in our review. There is a lack of robust positive findings on the genetics of early-onset BD in any major molecular genetics method. Limitations Early-onset populations were quite small in some studies. Variance in study methods hindered efforts to interpret results or conduct meta-analysis. Conclusions The field is still at an early phase for research on early-onset BD. The largely null findings mirror the results of most genetics research on BD. Although most studies were underpowered, the null findings could mean that early-onset BD may not be as genetically homogenous as has been hypothesized or even that early-onset BD does not differ genetically from adult-onset BD. Nevertheless, clinically the probabilistic developmental risk trajectories associated with early-onset that may not be primarily genetically determined continued to warrant scrutiny. Future research should dramatically expand sample sizes, use atheoretical research methods like GWAS, and standardize methods.

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“…Neurotransmitter systems examined in BD cell models include adrenergic (Berrettini et al, 1987b;Kay et al, 1993;Kay et al, 1994;Wright et al, 1984), serotonergic (Pinto et al, 2011) and cholinergic (Lin and Richelson, 1986;Nadi et al, 1984); most studies have had negative results. The binding of 125 I-iodohydroxybenzylpindolol to β-adrenoceptors in BD LCLs has been examined (Berrettini et al, 1987b;Kay et al, 1993;Kay et al, 1994;Wright et al, 1984), but only one study found lower binding in BD.…”

Section: Neurotransmitter and Neuroendocrine Systemsmentioning

confidence: 96%