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Recent Progress in Understanding the Pathophysiology of Post-Traumatic Stress Disorder: Implications for Targeted Pharmacological Treatment
Open accessAbstract
Post-traumatic stress disorder (PTSD) is a common and chronic anxiety disorder that can result after exposure to a traumatic event. Though our understanding of the aetiology of PTSD is incomplete, several neurobiological systems have been implicated in the pathophysiology and vulnerability towards developing PTSD after trauma exposure. We aimed to provide a concise review of benchmark findings in important neurobiological systems related to the aetiology and maintenance of PTSD symptomology. Specifically, we discuss functional aetiologies in the noradrenergic, serotonergic, endogenous cannabinoid and opioid systems as well as the hypothalamic-pituitary adrenal (HPA) axis. This article provides a succinct framework to appreciate the current understanding of neurobiological mechanisms related to the pathophysiology of PTSD and how these findings may impact the development of future, targeted pharmacological treatments for this debilitating disorder.
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“Other neuropeptides/neurotrophic factors, such as neuropeptide Y (95), dynorphin (96), and oxytocin as well as brain-derived neurotrophic factor (BDNF), are also involved in the HPA axis and in the orchestration of the response to stress.”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [96]
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Metadata
- Authors
- Bailey, C. R., Cordell, E., Sobin, S. M., & Neumeister, A.
- Affiliations
- Johns Hopkins University (US)
- NYU Langone Health (US)
- Corresponding author
- Neumeister, Alexander
- Venue
- CNS Drugs
- Published
- 2013-03
- Volume
- 27
- Issue
- 3
- Pages
- 221-232
- ISSN
- 1172-7047 (ISSN-L)
- 1179-1934
- PMC
- PMC3629370
- OpenAlex
- W2085725087
- Cited by
- 89
- References
- 203
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 4 · 2023: 8 · 2022: 4 · 2021: 10 · 2020: 9 · 2019: 9 · 2018: 7 · 2017: 7 · 2016: 8 · 2015: 7 · 2014: 7 · 2013: 2
- FWCI
- 1.17
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- CNS Drugs (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Mental Health (R21MH085627, R01MH096876, R21MH081103, R21MH096105)
- Topics
- Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Social Sciences › Psychology › Clinical Psychology › Psychoanalysis and Psychopathology Research
- Keywords
- post-traumatic stress disorder, pathophysiology, noradrenergic system, serotonergic system, endocannabinoid system, opioid system, hypothalamic-pituitary-adrenal axis, trauma exposure
- MeSH terms
- Animals, Female, Humans, Hypothalamo-Hypophyseal System, Male, Pituitary-Adrenal System, Stress Disorders, Post-Traumatic, Drug Design, Molecular Targeted Therapy
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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