Brain-Derived Neurotrophic Factor and Neuropsychiatric Disorders
Open accessAbstract
Brain derived neurotrophic factor (BDNF) is the most prevalent growth factor in the central nervous system (CNS). It is essential for the development of the CNS and for neuronal plasticity. Because BDNF plays a crucial role in development and plasticity of the brain, it is widely implicated in psychiatric diseases. This review provides a summary of clinical and preclinical evidence for the involvement of this ubiquitous growth factor in major depressive disorder, schizophrenia, addiction, Rett syndrome, as well as other psychiatric and neurodevelopmental diseases. In addition, the review includes a discussion of the role of BDNF in the mechanism of action of pharmacological therapies currently used to treat these diseases, such antidepressants and antipsychotics. The review also covers a critique of experimental therapies such as BDNF mimetics and discusses the value of BDNF as a target for future drug development.
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BDNF is a peptide of 118 highly conserved amino acids among vertebrates that regulates neuronal survival and synaptic plasticity in the adult brain and has been implicated in several neuropsychiatric disorders.
“Brain derived neurotrophic factor (BDNF) is a peptide consisting of 118 highly conserved amino acids among vertebrate species that regulates cellular and molecular mechanisms of neuronal survival and synaptic plasticity in the adult brain and has therefore been implicated in several neuropsychiatric disorders (Autry & Monteggia, 2012; Duman et al., 2016; Götz et al., 1992; Radziejewski et al., 199”
From Mechanisms of ketamine and its metabolites as antidepressants (2022) · cites this paper as Autry & Monteggia, 2012
The Introduction and “Brain-Derived Neurotrophic Factor Functions in Neurons” describe BDNF’s role in synaptic plasticity in the mature brain, neuronal survival, and neuropsychiatric disorders. The passages on BDNF’s structure and functions do not state that it consists of 118 amino acids or that its sequence is highly conserved among vertebrates; no page numbers are available in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredHPA-axis dysregulation is a key pathological feature of depression, and PBMC methylation is a potential biomarker.
“supporting HPA-axis dysregulation as a key pathological feature and highlighting PBMC methylation as a potential biomarker (Autry and Monteggia, 2012; Monteiro et al., 2017)”
From Histone modifications and depression: epigenetic mechanisms, therapeutic targets, and translational outlook (2026) · cites this paper as Autry and Monteggia, 2012
The section on BDNF expression in patients with depression (page unavailable) links the HPA axis to hippocampal stress responses in MDD, but does not describe HPA-axis dysregulation as a key pathological feature. The section on MDD and treatments discusses BDNF as a potential biomarker, not PBMC methylation; searches for PBMCs and peripheral-blood methylation found no supporting passage. (LLM, conf=0.83)
Experimental — accuracy not yet measuredReduced peripheral BDNF is consistently observed; although levels often increase with antidepressant treatment, their temporal trajectory does not always parallel symptom improvement.
“Reduced peripheral BDNF is consistently observed; although levels often increase with antidepressant treatment, their temporal trajectory does not always parallel symptom improvement, suggesting complex regulatory mechanisms (Autry and Monteggia, 2012; Monteiro et al., 2017).”
From Histone modifications and depression: epigenetic mechanisms, therapeutic targets, and translational outlook (2026) · cites this paper as Autry and Monteggia, 2012
The sections on BDNF expression in patients with depression and in patients treated with antidepressants report reduced serum BDNF in MDD and normalization after long-term treatment. They do not establish that the time course of peripheral BDNF changes sometimes fails to parallel symptom improvement. (LLM, conf=0.87)
Experimental — accuracy not yet measuredBDNF has been implicated in a number of psychiatric disorders, including schizophrenia, intellectual disability and autism, and the development of mood disorders such as depression and its treatment.
“BDNF has also been implicated in a number of psychiatric disorders, including schizophrenia, intellectual disability and autism, and the development of mood disorders such as depression and its treatment (Autry and Monteggia, 2012).”
From BDNF - a key transducer of antidepressant effects (2016) · cites this paper as Autry and Monteggia, 2012
The Schizophrenia section links BDNF to schizophrenia, and the sections on major depressive disorder and antidepressant treatment link it to depression and its treatment. The Rett Syndrome and Rubinstein–Taybi Syndrome sections discuss BDNF in conditions with autistic features and intellectual disability, respectively, but do not establish the broader claim about autism and intellectual disability as disorders in their own right. Page numbers were not available in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredChronic stress decreases BDNF expression in the hippocampus and prefrontal cortex, contributing to neuronal atrophy observed in depression.
“Chronic stress, a well-established risk factor for MDD, has been shown to decrease BDNF expression in critical brain regions such as the hippocampus and prefrontal cortex (PFC), contributing to the neuronal atrophy observed in depression [2,22,33].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [22]
The section on human patients with depression links reduced BDNF to hippocampal structural changes, but says those changes *may* be attributed in part to reduced BDNF and TrkB. It reports a correlation between reduced prefrontal volume and BDNF levels, not that reduced BDNF causes prefrontal atrophy. Figure 2 depicts BDNF down-regulation in the hippocampus and cortex with MDD or stress. (LLM, conf=0.82)
Experimental — accuracy not yet measured
Mature BDNF and pro-BDNF trigger distinct intracellular signaling pathways.
“Mature BDNF and its precursor pro-BDNF trigger distinct intracellular signaling pathways [22,23].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [22]
Section A states that recent data suggest pro-BDNF and mature BDNF activate different intracellular signaling pathways, and describes their different receptors. The citing sentence presents that suggested distinction as an established fact, omitting the source's qualification. (LLM, conf=0.84)
Experimental — accuracy not yet measuredBDNF is critical for synaptic plasticity, neurogenesis, and neuronal survival, and its altered expression is implicated in the development of depressive symptoms.
“BDNF is critical for synaptic plasticity, neurogenesis, and neuronal survival, and its altered expression has been implicated in the development of depressive symptom [2,22].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [22]
The section “Brain-Derived Neurotrophic Factor Functions in Neurons” states that BDNF is essential for synaptic plasticity and required for the survival of several types of neurons. The section on human patients with depression links altered, region-specific BDNF expression to MDD. But the section “Association of Brain-Derived Neurotrophic Factor and Neurogenesis in Depression and Antidepressant Treatment?” reports normal neurogenesis in BDNF-deficient mice and does not establish that BDNF is critical for neurogenesis. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThe BDNF-TrkB signaling pathway has a potential direct effect in the mechanism of action of antidepressants.
“These results highlight the potential direct effect of the BDNF-TrkB signaling pathway in the mechanism of action of antidepressants (Autry and Monteggia 2012)”
From Neurotrophic factors and neuroplasticity pathways in the pathophysiology and treatment of depression (2018) · cites this paper as Autry and Monteggia 2012
Mature BDNF interacts with the high-affinity TrkB receptor.
“In contrast, mature BDNF interacts with the high-affinity tropomyosin receptor kinase B (TrkB) receptor and other signaling pathways [22].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [22]
Taken together, these findings suggest a complex role for BDNF signaling in MDD, with increased activity in the amygdala and nucleus accumbens and decreased activity in the hippocampus and prefrontal cortex.
“Taken together, these findings suggest a complex role for BDNF signaling in MDD, with increased activity in the amygdala and nucleus accumbens and decreased activity in the hippocampus and prefrontal cortex [22].”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [22]
BDNF is produced as a precursor protein proBDNF, which is subsequently cleaved into its mature, biologically active form.
“It is produced as a precursor protein known as proBDNF, which is subsequently cleaved into its mature, biologically active form.”
From Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review (2024) · cites this paper as [22]
The effects of antidepressant drugs on BDNF synthesis and TrkB signaling have been well characterized.
“In particular, the effects of antidepressant drugs on BDNF synthesis and TrkB signaling have been well-characterized102–105, yet these effects have been largely ignored by the pharmaceutical industry and clinical development.”
From Neuronal plasticity and neurotrophic factors in drug responses (2017) · cites this paper as [103]
There are safe and widely used drugs already on the market that increase BDNF production or TrkB activation in the brain.
“It is, therefore, remarkable that there actually are safe and widely used drugs already in market that increase the production of BDNF or the activation of TrkB in brain.”
From Neuronal plasticity and neurotrophic factors in drug responses (2017) · cites this paper as [103]
Neurodegenerative and neuropsychiatric diseases may be partially caused by defects in synaptic plasticity associated with insufficient neuronal supply of BDNF and other neurotrophic factors.
“Furthermore, it was shown that neurodegenerative and neuropsychiatric diseases may be partially caused by defects in synaptic plasticity associated with the insufficient neuronal supply of BDNF and other neurotrophic factors [11,12,13].”
From BDNF as a Promising Therapeutic Agent in Parkinson’s Disease (2020) · cites this paper as [12]
Patients with psychiatric and neurodegenerative disorders often have reduced BDNF concentrations in their blood and brain.
“Patients with psychiatric and neurodegenerative disorders often have reduced BDNF concentrations in their blood and brain.”
From Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation (2019) · cites this paper as [22]
BDNF is a growth factor that regulates neurite outgrowth, functional neuronal connections, synapse formation and synaptic plasticity in the central nervous system.
“Brain-derived neurotrophic factor (BDNF) is a growth factor that regulates neurite outgrowth, functional neuronal connections, synapse formation and synaptic plasticity in the central nervous system 149–152.”
From Mechanisms of ketamine action as an antidepressant (2018) · cites this paper as [149]
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Putative neural consequences of captivity for elephants and cetaceans
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Boulle, F., Velthuis, H., Koedam, K., Steinbusch, H. W., van den Hove, D. L. A., Kenis, G., Gabriel, C., Mocaer, E., Franc, B., Rognan, D., et al. (2016) · European Neuropsychopharmacology · doi:10.1016/j.euroneuro.2015.11.003 · Cited by 24 · see citing works
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Quest for biomarkers of treatment-resistant depression: Shifting the paradigm toward risk
Smith, D. F. (2013) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2013.00057 · Cited by 22 · see citing works
Reyes, S. T., Deacon, R. M. J., Guo, S. G., Altimiras, F. J., Castillo, J. B., van der Wildt, B., Morales, A. P., Park, J. H., Klamer, D., Rosenberg, J., et al. (2021) · Scientific Reports · doi:10.1038/s41598-021-94079-7 · Cited by 22 · see citing works
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Serum BDNF levels increase during early drug withdrawal in alcohol and crack cocaine addiction
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“…FKBP5 hypomethylation with increased expression correlate with depression severity and suicidal ideation (Roy et al., 2017), supporting HPA-axis dysregulation as a key pathological feature and highlighting PBMC methylation as a potential biomarker (Autry and Monteggia, 2012; Monteiro et al., 2017).”
BDNF promoter methylation and genetic variation in late-life depression
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- Authors
- Autry, A. E., & Monteggia, L. M.
- Affiliations
- The University of Texas Southwestern Medical Center (US)
- Venue
- Pharmacological Reviews
- Publisher
- Elsevier BV
- Published
- 2012-04
- Volume
- 64
- Issue
- 2
- Pages
- 238-258
- ISSN
- 0031-6997 (ISSN-L)
- PMC
- PMC3310485
- OpenAlex
- W2110696099
- Cited by
- 1,390
- References
- 232
- Citations by year
- 2026: 68 · 2025: 96 · 2024: 98 · 2023: 94 · 2022: 102 · 2021: 114 · 2020: 110 · 2019: 135 · 2018: 120 · 2017: 95 · 2016: 110 · 2015: 77 · 2014: 79 · 2013: 61 · 2012: 28
- FWCI
- 8.28
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Pharmacological Reviews (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (MH070727, MH081060)
- National Institute of Mental Health (MH 070727, R01MH081060, MH081060, R01MH070727)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- brain-derived neurotrophic factor, neuropsychiatric disorders, major depressive disorder, schizophrenia, addiction, Rett syndrome, neurodevelopmental disorders, neuroplasticity, antidepressants, antipsychotic drugs, BDNF mimetic, drug development
- MeSH terms
- Animals, Antidepressive Agents, Mental Disorders, Humans, Nervous System Diseases, Neuronal Plasticity, Antipsychotic Agents, Drug Design, Drug Delivery Systems, Brain-Derived Neurotrophic Factor
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.
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