Genetic variants within the serotonin transporter associated with familial risk for major depression

Talati, Ardesheer; Guffanti, Guia; Odgerel, Zagaa; Ionita‐Laza, Iuliana; Malm, Heli; Sourander, André; Brown, Alan S.; Wickramaratne, Priya; Gingrich, Jay A.; Weissman, Myrna M.

doi:10.1016/j.psychres.2015.04.015

Cited by 14 publications

(11 citation statements)

References 24 publications

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“…Recent research demonstrates that relative to low-risk probands, offspring at high familial risk of MDD are four times more likely to be carriers of the 5-HTTLPR S allele (Talati et al, 2015). These findings support other studies and meta-analyses which suggest a relationship between the 5-HTTLPR S allele and MDD risk (Bogdan, Agrawal, Gaffrey, Tillman, & Luby, 2014;Kim et al, 2007;Kiyohara & Yoshimasu, 2010), although other meta-analyses have failed to replicate this finding (e.g.…”

Section: The Role Of Amygdala Function In Depressionsupporting

confidence: 68%

“…As previously discussed, there is a probable link between the 5-HTTLPR S allele and MDD vulnerability (Munafò, Durrant, Lewis, & Flint, 2009;Talati et al, 2015; however see: Risch et al, 2009), which may be related to altered patterns of functional amygdala activity (Costafreda et al, 2013). There is also abundant evidence to suggest that amygdala hyperactivity towards negative stimuli is related to long-term negative memory bias in depression (Hamilton & Gotlib, 2008).…”

Section: The 'Affect Tagging and Consolidation' (Atac) Modelmentioning

confidence: 97%

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The ‘affect tagging and consolidation’ (ATaC) model of depression vulnerability

Harrington

Pennington

Durrant

2017

Neurobiology of Learning and Memory

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Please cite this article as: Harrington, M.O., Pennington, K., Durrant, S.J., The 'Affect Tagging and Consolidation' (ATaC) Model of Depression Vulnerability, Neurobiology of Learning and Memory (2017), doi: http://dx.doi.org/10. 1016/j.nlm.2017.02.003 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. patients, suggesting that they may be vulnerability markers of major depressive disorder (MDD), rather than mere epiphenomena of the disorder. Neuroimaging studies have revealed that depression is also associated with heightened amygdala reactivity to negative emotional stimuli, which may also be a vulnerability marker for MDD. Several models have been developed to explain the respective roles of REM sleep alterations and negatively-biased amygdala activity in the pathology of MDD, however the possible interaction between these two potential risk-factors remains uncharted. This paper reviews the roles of the amygdala and REM sleep in the encoding and consolidation of negative emotional memories, respectively. We present our 'affect tagging and consolidation' (ATaC) model, which argues that increased REM sleep density and negatively-biased amygdala activity are two separate, genetically influenced risk-factors for depression which interact to promote the development of negative memory bias -a well-known cognitive vulnerability marker for depression.Predictions of the ATaC model may motivate research aimed at improving our understanding of sleep dependent memory consolidation in depression aetiology.

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Section: The Role Of Amygdala Function In Depressionsupporting

confidence: 68%

Section: The 'Affect Tagging and Consolidation' (Atac) Modelmentioning

confidence: 97%

The ‘affect tagging and consolidation’ (ATaC) model of depression vulnerability

Harrington

Pennington

Durrant

2017

Neurobiology of Learning and Memory

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“…A recessive model best explained the data, with high risk offspring 3-4 times more likely to have both copies of short allele (SS). 21 5 HTTLPR-rs25531DEFICIwas not significantly association with familial risk. However offspring with two low functional variants had higher rate of MDD.…”

Section: Serotoninmentioning

confidence: 78%

A Review on Diagnostic Proteomics of Depression

Samad¹

2017

MOJPB

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Depression is the psychiatric disorder cause when deviation occurs from the standard proteomic condition in individuals. Pathogenesis and etiology of psychiatric disorders are still not clear and many signaling pathways are unknown. In that case the gene provides the primary information about expression of gene and activities of brain. This review focused on the diagnostic proteomics of depression by means of biomarkers. Evidences suggested that reduced and elevated levels of these biomarkers involved in the pathology of depression. These biomarkers could not be used for the diagnostic purposes but also used for the therapeutics. The aim of this non-systematic review article is to evaluate and document a potential importance of proteomics in diagnosis of depression.

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“…For analysis of the effects of SLC6A4 alleles on each parameter, these alleles were divided into three groups defined by the presence of the L allele or the L G allele in a ‘dose-dependent' manner: S/S (dose = 0), L/S (dose = 1), L/L (dose = 2), or S (L G )/S (L G ) (dose = 0), L A /S (L G ) (dose = 1), L A /L A (dose = 2) [50,51]. SLC6A4 mRNA expression levels, methylation rates in each CpG site, and the participant's age were compared between AD and control subjects with the Student t test or Mann-Whitney U test after the Shapiro-Wilk test.…”

Section: Methodsmentioning

confidence: 99%

Association Study and Meta-Analysis of Polymorphisms, Methylation Profiles, and Peripheral mRNA Expression of the Serotonin Transporter Gene in Patients with Alzheimer's Disease

Yamazaki

Yoshino²,

Mori³

et al. 2016

Dement Geriatr Cogn Disord

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Background/Aim: The aim of this study was to elucidate the relationship between Alzheimer's disease (AD) and the serotonin transporter gene (SLC6A4). Methods: AD subjects (n = 43) and controls (n = 47) were recruited and evaluated. In leukocytes, we evaluated two polymorphisms in SLC6A4, the serotonin transporter length polymorphic region (5-HTT-LPR) and rs25531, as well as methylation rates of the SLC6A4 promoter region and the SLC6A4 mRNA expression level. We also performed a meta-analysis to examine the relationship between the frequency of the L allele and the risk of AD. Results: The distributions of 5-HTT-LPR and rs25531 polymorphisms in AD subjects were not different from those of controls. Although the methylation rates in AD subjects were not significantly different from those of controls, the expression level in AD subjects was significantly higher than in controls. Additionally, the expression level in AD subjects was significantly correlated with apathy. Meta-analysis revealed that the L/L genotype significantly reduced the risk of AD, but only in the Caucasian population. Conclusion: Higher SLC6A4 mRNA expression in leukocytes in AD was associated with apathy regardless of SLC6A4 genotypes and methylation rates of the promoter region. The L/L genotype may reduce the risk of AD in the Caucasian population.

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Genetic variants within the serotonin transporter associated with familial risk for major depression

Cited by 14 publications

References 24 publications

The ‘affect tagging and consolidation’ (ATaC) model of depression vulnerability

The ‘affect tagging and consolidation’ (ATaC) model of depression vulnerability

A Review on Diagnostic Proteomics of Depression

Association Study and Meta-Analysis of Polymorphisms, Methylation Profiles, and Peripheral mRNA Expression of the Serotonin Transporter Gene in Patients with Alzheimer's Disease

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