Pathways underlying neuroprogression in bipolar disorder: Focus on inflammation, oxidative stress and neurotrophic factors
Abstract
There is now strong evidence of progressive neuropathological processes in bipolar disorder (BD). On this basis, the current understanding of the neurobiology of BD has shifted from an initial focus on monoamines, subsequently including evidence of changes in intracellular second messenger systems and more recently to, incorporating changes in inflammatory cytokines, corticosteroids, neurotrophins, mitochondrial energy generation, oxidative stress and neurogenesis into a more comprehensive model capable of explaining some of the clinical features of BD. These features include progressive shortening of the inter-episode interval with each recurrence, occurring in consort with reduced probability of treatment response as the illness progresses. To this end, emerging data shows that these biomarkers may differ between early and late stages of BD in parallel with stage-related structural and neurocognitive alterations. This understanding facilitates identification of rational therapeutic targets, and the development of novel treatment classes. Additionally, these pathways provide a cogent explanation for the efficacy of seemingly diverse therapies used in BD, that appear to share common effects on oxidative, inflammatory and neurotrophic pathways.
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Increased oxidative damage occurs quite often in bipolar disorder.
“bipolar disorder (BD) [10–14]”
From Oxidative Stress Implications in the Affective Disorders: Main Biomarkers, Animal Models Relevance, Genetic Perspectives, and Antioxidant Approaches (2016) · cites this paper as [14]
There is strong evidence that inflammation and oxidative stress underlie the progression of depression, anxiety and bipolar disorder.
“There is strong evidence that inflammation and oxidative stress underlie the progression of depression, anxiety and bipolar disorder (Berk et al., 2011; Milaneschi et al., 2021).”
From An application of the stress-diathesis model: A review about the association between smoking tobacco, smoking cessation, and mental health (2023) · cites this paper as Berk et al., 2011
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Tobacco use in bipolar disorder
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Self-citation
- Authors
- Berk, M., Kapczinski, F., Andreazza, A. C., Dean, O. M., Giorlando, F., Maes, M., Yücel, M., Gama, C. S., Dodd, S., Dean, B., Magalhães, P. V. S., Amminger, P., McGorry, P., & Malhi, G. S.
- Affiliations
- Barwon Health (AU)
- Universidade Federal do Rio Grande do Sul (BR)
- Mental Health Research Institute (AU)
- Piyavate Hospital (TH)
- The University of Melbourne (AU)
- The University of Sydney (AU)
- Corresponding author
- Berk, M.
- ORCID
- Venue
- Neuroscience & Biobehavioral Reviews
- Publisher
- Elsevier BV
- Published
- 2011-01
- Volume
- 35
- Issue
- 3
- Pages
- 804-817
- ISSN
- 0149-7634 (ISSN-L)
- OpenAlex
- W2142476463
- Cited by
- 1,178
- References
- 214
- Citations by year
- 2026: 49 · 2025: 50 · 2024: 50 · 2023: 54 · 2022: 56 · 2021: 70 · 2020: 95 · 2019: 82 · 2018: 89 · 2017: 90 · 2016: 103 · 2015: 110 · 2014: 89 · 2013: 92 · 2012: 69
- FWCI
- 8.66
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience & Biobehavioral Reviews (publishedVersion)
- PubMed (publishedVersion)
- Swinburne figshare (Swinburne University of Technology) (submittedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Bipolar Disorder and Treatment
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Keywords
- bipolar disorder, neuroprogression, neuroinflammation, oxidative stress, neurotrophic factors, neurotrophins, inflammatory cytokines, corticosteroids, mitochondrial bioenergetics, neurogenesis, treatment response, biomarkers, brain structural changes, neurocognitive impairment, therapeutic target
- MeSH terms
- Animals, Bipolar Disorder, Humans, Inflammation, Nerve Growth Factors, Cytokines, Neurotransmitter Agents, Oxidative Stress, Disease Progression, Neuroprotective Agents
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