The Genetic Basis of Panic Disorder
Open accessAbstract
Panic disorder is one of the chronic and disabling anxiety disorders. There has been evidence for either genetic heterogeneity or complex inheritance, with environmental factor interactions and multiple single genes, in panic disorder's etiology. Linkage studies have implicated several chromosomal regions, but no research has replicated evidence for major genes involved in panic disorder. Researchers have suggested several neurotransmitter systems are related to panic disorder. However, to date no candidate gene association studies have established specific loci. Recently, researchers have emphasized genome-wide association studies. Results of two genome-wide association studies on panic disorder failed to show significant associations. Evidence exists for differences regarding gender and ethnicity in panic disorder. Increasing evidence suggests genes underlying panic disorder overlap, transcending current diagnostic boundaries. In addition, an anxious temperament and anxiety-related personality traits may represent intermediate phenotypes that predispose to panic disorder. Future research should focus on broad phenotypes, defined by comorbidity or intermediate phenotypes. Genome-wide association studies in large samples, studies of gene-gene and gene-environment interactions, and pharmacogenetic studies are needed.
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The implication of the most common COMT polymorphism in PD is controversial due to extremely different study results.
“The implication of the most common COMT polymorphism in PD is also rather controversial due to extremely different study results (reviewed by [205]).”
From Oxidative Stress Implications in the Affective Disorders: Main Biomarkers, Animal Models Relevance, Genetic Perspectives, and Antioxidant Approaches (2016) · cites this paper as [205]
Association analyses of PD genetics showed classical candidates such as MAOA, COMT, ADORA2A, and CCK-BR genes.
“Association analyses of PD genetics showed several classical candidates such as monoamine oxidase A (MAOA), catechol-O-methyl transferase (COMT), adenosine A2A receptor (ADORA2A), and cholecystokinin B receptor (CCK-BR) genes [205].”
From Oxidative Stress Implications in the Affective Disorders: Main Biomarkers, Animal Models Relevance, Genetic Perspectives, and Antioxidant Approaches (2016) · cites this paper as [205]
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- Authors
- Na, H.-R., Kang, E.-H., Lee, J.-H., & Yu, B.-H.
- Affiliations
- Samsung Medical Center (KR)
- Corresponding author
- Yu, Bum-Hee
- ORCID
- Kang, Eun-Ho
- Venue
- Journal of Korean Medical Science
- Publisher
- Korean Academy of Medical Sciences
- Published
- 2011
- Volume
- 26
- Issue
- 6
- Pages
- 701
- ISSN
- 1011-8934 (ISSN-L)
- 1598-6357
- PMC
- PMC3102861
- OpenAlex
- W2103043509
- Cited by
- 27
- References
- 88
- Citations by year
- 2025: 1 · 2024: 2 · 2022: 4 · 2020: 2 · 2019: 1 · 2018: 2 · 2016: 4 · 2015: 3 · 2013: 3 · 2012: 5
- FWCI
- 0.34
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Journal of Korean Medical Science (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Topics
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Anxiety, Depression, Psychometrics, Treatment, Cognitive Processes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- panic disorder, genetic etiology, anxiety disorders, genetic heterogeneity, multifactorial inheritance, linkage analysis, candidate gene association, genome-wide association study, neurotransmitter systems, gender differences, ethnic differences, endophenotypes, anxious temperament, gene-environment interaction, pharmacogenetics
- MeSH terms
- Catechol O-Methyltransferase, Cholecystokinin, Humans, Monoamine Oxidase, Panic Disorder, Genome-Wide Association Study, Genetic Loci
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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.
Statistics and arithmetic are recomputed, not judged.
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