Overview of the Genetics of Major Depressive Disorder
Open accessAbstract
Major depressive disorder (MDD) is a common psychiatric illness with high levels of morbidity and mortality. Despite intensive research during the past several decades, the neurobiological basis and pathophysiology of depressive disorders remain unknown. Genetic factors play important roles in the development of MDD, as indicated by family, twin, and adoption studies, and may reveal important information about disease mechanisms. This article describes recent developments in the field of psychiatric genetics, with a focus on MDD. Early twin studies, linkage studies, and association studies are discussed. Recent findings from genome-wide association studies are reviewed and future directions discussed. Despite all efforts, thus far, no single genetic variation has been identified to increase the risk of depression substantially. Genetic variants are expected to have only small effects on overall disease risk, and multiple genetic factors in conjunction with environmental factors are likely necessary for the development of MDD. Future large-scale studies are needed to dissect this complex phenotype and to identify pathways involved in the etiology of MDD.
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Family, twin, and adoption studies suggest that genetic factors play a crucial role in the occurrence of MDD.
“Recent family, twin, and adoption studies suggests that genetic factors play a crucial role in the occurrence of MDD. 25”
From Major depressive disorder: hypothesis, mechanism, prevention and treatment (2024) · cites this paper as [25]
Stressful social events are capable of serving as triggers for epigenetic alterations at specific gene loci, potentially causing long-term changes in brain functioning.
“stressful social events are capable of serving as triggers for epigenetic alterations at specific gene loci, potentially causing long-term changes in brain functioning (Lohoff, 2010).”
From Social functioning in major depressive disorder (2016) · cites this paper as Lohoff, 2010
Tryptophan hydroxylase gene encodes for an important rate-limiting enzyme of brain serotonin synthesis and is thought to be implicated in DD.
“Another gene thought to be implicated in DD is tryptophan hydroxylase gene, which encodes for an important rate-limiting enzyme of brain serotonin synthesis [231].”
From Oxidative Stress Implications in the Affective Disorders: Main Biomarkers, Animal Models Relevance, Genetic Perspectives, and Antioxidant Approaches (2016) · cites this paper as [231]
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- Authors
- Lohoff, F. W.
- Affiliations
- University of Pennsylvania (US)
- Corresponding author
- Lohoff, Falk W.
- ORCID
- Lohoff, Falk W.
- Venue
- Current Psychiatry Reports
- Published
- 2010-09-17
- Volume
- 12
- Issue
- 6
- Pages
- 539-546
- ISSN
- 1523-3812 (ISSN-L)
- 1535-1645
- PMC
- PMC3077049
- OpenAlex
- W2046955370
- Cited by
- 498
- References
- 62
- Citations by year
- 2026: 15 · 2025: 24 · 2024: 24 · 2023: 62 · 2022: 45 · 2021: 27 · 2020: 65 · 2019: 26 · 2018: 38 · 2017: 39 · 2016: 28 · 2015: 25 · 2014: 21 · 2013: 17 · 2012: 31
- FWCI
- 2.00
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Current Psychiatry Reports (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (K08MH080372)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- major depressive disorder, genetic susceptibility, psychiatric genetics, twin studies, family studies, adoption studies, genetic linkage, genome-wide association study, genetic variants, gene-environment interaction, depression pathophysiology
- MeSH terms
- Depressive Disorder, Major, Major Depressive Disorder, Humans, Genetic Linkage, Tryptophan Hydroxylase, Twin Studies as Topic, Brain-Derived Neurotrophic Factor, Genetic Predisposition to Disease, Receptor, Serotonin, 5-HT2A, Serotonin Plasma Membrane Transport Proteins, Genetic Association Studies
About these checks
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.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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