Brain-derived neurotrophic factor: role in depression and suicide
Open accessAbstract
Depression and suicidal behavior have recently been shown to be associated with disturbances in structural and synaptic plasticity. Brain-derived neurotrophic factor (BDNF), one of the major neurotrophic factors, plays an important role in the maintenance and survival of neurons and in synaptic plasticity. Several lines of evidence suggest that BDNF is involved in depression, such that the expression of BDNF is decreased in depressed patients. In addition, antidepressants up-regulate the expression of BDNF. This has led to the proposal of the "neurotrophin hypothesis of depression". Increasing evidence demonstrates that suicidal behavior is also associated with lower expression of BDNF, which may be independent from depression. Recent genetic studies also support a link of BDNF to depression/suicidal behavior. Not only BDNF, but abnormalities in its cognate receptor tropomycin receptor kinase B (TrkB) and its splice variant (TrkB.T1) have also been reported in depressed/suicidal patients. It has been suggested that epigenetic modulation of the Bdnf and Trkb genes may contribute to their altered expression and functioning. More recently, impairment in the functioning of pan75 neurotrophin receptor has been reported in suicide brain specimens. pan75 neurotrophin receptor is a low-affinity neurotrophin receptor that, when expressed in conjunction with low availability of neurotropins/Trks, induces apoptosis. Overall, these studies suggest the possibility that BDNF and its mediated signaling may participate in the pathophysiology of depression and suicidal behavior. This review focuses on the critical evidence demonstrating the involvement of BDNF in depression and suicide.
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Stress and depression decrease the expression and function of BDNF in prefrontal cortex and hippocampus, as well as decrease the levels in the blood of depressed patients.
“Stress and depression decrease the expression and function of BDNF (Figure 2) in prefrontal cortex and hippocampus, structures implicated in depression, as well as decrease the levels in the blood of depressed patients21,32–35.”
From Synaptic plasticity and depression: new insights from stress and rapid-acting antidepressants (2016) · cites this paper as [34]
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References 240 · Cited by 355
Research works printed but not linked: 2
- [1]World Health Organization The global burden of disease Geneva, Switzerland World Health Organization Press 1996
- [2]Blazer DG Mood disorders: epidemiology, in Comprehensive Textbook of Psychiatry Sadock BJ Sadock VA Lippincott Williams & Wilkins New York 2000 1298 1308
- Authors
- Dwivedi, Y.
- Affiliations
- University of Illinois Chicago (US)
- Corresponding author
- Dwivedi, Yogesh
- ORCID
- Dwivedi, Yogesh
- Venue
- Neuropsychiatric Disease and Treatment
- Publisher
- Informa UK Limited
- Published
- 2009-08
- Volume
- 5
- Pages
- 433
- ISSN
- 1176-6328 (ISSN-L)
- PMC
- PMC2732010
- OpenAlex
- W2014381681
- Cited by
- 355
- References
- 240
- Citations by year
- 2026: 7 · 2025: 23 · 2024: 27 · 2023: 28 · 2022: 32 · 2021: 28 · 2020: 21 · 2019: 19 · 2018: 19 · 2017: 20 · 2016: 16 · 2015: 26 · 2014: 22 · 2013: 22 · 2012: 12
- FWCI
- 10.54
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Neuropsychiatric Disease and Treatment (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Dove Medical Press (Taylor and Francis Group) (submittedVersion, cc-by-nc)
- Funders
- American Foundation for Suicide Prevention (R21MH081099, R0168777)
- National Institute of Mental Health (R21MH081099, R0168777, R01MH082802)
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- brain-derived neurotrophic factor, depression, suicide, synaptic plasticity, antidepressants, TrkB receptor, epigenetic regulation, neuronal apoptosis, gene expression
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