Serotonin Transporter (5-HTTLPR) Genotype and Amygdala Activation: A Meta-Analysis
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Background We evaluated the magnitude of the reported associations between amygdala activation and the serotonin transporter gene linked polymorphic region (5-HTTLPR) and the likely effect size of this relationship.Methods We used meta-analytic techniques to combine data from existing published and unpublished studies. We also tested for possible publication bias and explored possible moderating influences on any association, such as sample ancestry.Results Our results provide support for the association of the 5-HTTLPR polymorphism and amygdala activation and suggest that this locus may account for up to 10% of phenotypic variance. Although we did not observe evidence for potential publication bias in our main analysis, this was due in part to efforts to obtain unpublished data pertinent to this meta-analysis, and when three unpublished data sets were excluded we did observe evidence of such bias. We also observed evidence that the first published study may provide an overestimate of the true effect size, which is consistent with findings from genetic association studies of other phenotypes.Conclusions Although our analysis provides support for the association of the 5-HTTLPR polymorphism and amygdala activation, it also suggests that most studies to date are nevertheless lacking in statistical power. Increasing the sample sizes of future imaging genetics studies will allow a more accurate characterization of any true effect size and afford adequate power to examine the impact of multiple polymorphisms that likely work in concert to affect gene function and, in turn, bias neural processes mediating dispositional traits such as temperament and personality.
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S-carriers have increased amygdala activation to fearful faces or threatening stimuli in most studies.
“S-carriers have been reported to have increased amygdala activation to fearful faces or threatening stimuli in most studies and a meta-analysis of 14 studies concluded that it might account for up to 10% of the variance (Munafo et al., 2008).”
From Affective Cognition and its Disruption in Mood Disorders (2011) · cites this paper as Munafo et al., 2008
A meta-analysis of 14 studies concluded that S-carrier status might account for up to 10% of the variance in amygdala activation.
“S-carriers have been reported to have increased amygdala activation to fearful faces or threatening stimuli in most studies and a meta-analysis of 14 studies concluded that it might account for up to 10% of the variance (Munafo et al., 2008).”
From Affective Cognition and its Disruption in Mood Disorders (2011) · cites this paper as Munafo et al., 2008
Munafo et al. (2008) conducted a meta-analysis of studies reporting associations between a VNTR polymorphism in the serotonin transporter gene (5-HTTLPR) and amygdala activation and suggested that an imaging genetics study would require a total sample of about 70 participants to achieve .8 power for an alpha power of .05.
“For example,Munafo et al. (2008) conducted a meta-analysis of studies that have reported associations between a VNTR polymorphism in the serotonin transporter gene (5-HTTLPR) and amygdala activation and suggested that an imaging genetics study would require a total sample of about 70 participants to achieve .8 power for an alpha power of .05.”
From Developmental imaging genetics: Linking dopamine function to adolescent behavior (2014) · cites this paper as Munafo et al. (2008)
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- Authors
- Munafò, M. R., Brown, S. M., & Hariri, A. R.
- Affiliations
- University of Pittsburgh (US)
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2008-05
- Volume
- 63
- Issue
- 9
- Pages
- 852-857
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC2755289
- OpenAlex
- W1991731575
- Cited by
- 789
- References
- 49
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 3 · 2023: 11 · 2022: 10 · 2021: 36 · 2020: 52 · 2019: 23 · 2018: 23 · 2017: 26 · 2016: 41 · 2015: 56 · 2014: 51 · 2013: 73 · 2012: 97
- FWCI
- 5.14
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Explore Bristol Research (publishedVersion)
- PubMed Central (acceptedVersion)
- Bristol Research (University of Bristol) (submittedVersion)
- Funders
- National Alliance for Research on Schizophrenia and Depression
- National Institutes of Health
- National Institute of Mental Health (K01MH072837)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Keywords
- serotonin transporter gene, 5-HTTLPR polymorphism, amygdala activation, imaging genetics, genetic association, publication bias, effect size, temperament, personality, neuroimaging
- MeSH terms
- Adolescent, Adult, Alleles, Amygdala, Anxiety Disorders, Depressive Disorder, Female, Genotype, Humans, Individuality, Magnetic Resonance Imaging, Male, Phenotype, Polymorphism, Genetic, Promoter Regions, Genetic, Stress, Psychological, Serotonin Plasma Membrane Transport Proteins
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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