ReviewFrontiers in behavioral neuroscience2021
Concepts of Neuroinflammation and Their Relationship With Impaired Mitochondrial Functions in Bipolar Disorder.
Review in Frontiers in behavioral neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Pharmacotherapeutic Options in Drug-Resistant Bipolar Depression: From Molecular Mechanisms to Rational Polypharmacotherapy.Biomedicines · 2026Review
- Mitochondrial dynamics in depression: friend or foe?Metabolic brain disease · 2026Review
- Flavonoids as Modulators of Neuroinflammation in Affective Disorders: A Narrative Review.International journal of molecular sciences · 2026Review
- Neuroprotective Effects of Strength Training on Behavioral Deficit, Oxidative Damage, Astrogliosis, and Neuronal Death in a Bipolar Disorder Model.Journal of neurochemistry · 2026Article
- Metabolic reprogramming in sepsis-associated encephalopathy: emerging mechanisms, candidate biomarkers, and future therapeutic directions.Frontiers in medicine · 2026Review
- The Breathomics Profile of Volatile Sulfur Compounds in the Bipolar Spectrum, Does It Represent a Potential Tool for Early Diagnosis?Journal of clinical medicine · 2025Article
- Altered serum interleukin-17A and interleukin-23A levels may be associated with the pathophysiology and development of generalized anxiety disorder.Scientific reports · 2024Article
- Effect of antipsychotics and mood stabilisers on metabolism in bipolar disorder: a network meta-analysis of randomised-controlled trials.EClinicalMedicine · 2024Article
- Mitochondrial dysfunction in chronic neuroinflammatory diseases (Review).International journal of molecular medicine · 2024Review
- Boltzmann's Theorem Revisited: Inaccurate Time-to-Action Clocks in Affective Disorders.Current neuropharmacology · 2024Review
- Exploring hub genes and crucial pathways linked to oxidative stress in bipolar disorder depressive episodes through bioinformatics analysis.Frontiers in psychiatry · 2024Article
- Vitamin D Status in Bipolar Disorder.Nutrients · 2023Article
- Shifting levels of peripheral inflammatory profiles as an indicator for comorbid multiple autoimmune diseases and bipolar disorder: a case report.BMC psychiatry · 2023Article
- Does treatment with autophagy-enhancers and/or ROS-scavengers alleviate behavioral and neurochemical consequences of low-dose rotenone-induced mild mitochondrial dysfunction in mice?Molecular psychiatry · 2023Article
- Endo-Lysosomal and Autophagy Pathway and Ubiquitin-Proteasome System in Mood Disorders: A Review Article.Neuropsychiatric disease and treatment · 2023Review
- Neuroinflammation and neuroprogression produced by oxidative stress in euthymic bipolar patients with different onset disease times.Scientific reports · 2022Article
- Therapeutic Interventions to Mitigate Mitochondrial Dysfunction and Oxidative Stress-Induced Damage in Patients with Bipolar Disorder.International journal of molecular sciences · 2022Review
- Helicid Improves Lipopolysaccharide-Induced Apoptosis of C6 Cells by Regulating SH2D5 DNA Methylation via the CytC/Caspase9/Caspase3 Signaling Pathway.Contrast media & molecular imaging · 2022Article
- Editorial: Neurobiological Underpinnings of Bipolar Disorder and Its Treatment.Frontiers in psychiatry · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bipolar disorder (BD) is a chronic psychiatric disease, characterized by frequent behavioral episodes of depression and mania, and neurologically by dysregulated neurotransmission, neuroplasticity, growth factor signaling, and metabolism, as well as oxidative stress, and neuronal apoptosis, contributing to chronic neuroinflammation. These abnormalities result from complex interactions between multiple susceptibility genes and environmental factors such as stress. The neurocellular abnormalities of BD can result in gross morphological changes, such as reduced prefrontal and hippocampal volume, and circuit reorganization resulting in cognitive and emotional deficits. The term "neuroprogression" is used to denote the progressive changes from early to late stages, as BD severity and loss of treatment response correlate with the number of past episodes. In addition to circuit and cellular abnormalities, BD is associated with dysfunctional mitochondria, leading to severe metabolic disruption in high energy-demanding neurons and glia. Indeed, mitochondrial dysfunction involving electron transport chain (ETC) disruption is considered the primary cause of chronic oxidative stress in BD. The ensuing damage to membrane lipids, proteins, and DNA further perpetuates oxidative stress and neuroinflammation, creating a perpetuating pathogenic cycle. A deeper understanding of BD pathophysiology and identification of associated biomarkers of neuroinflammation are needed to facilitate early diagnosis and treatment of this debilitating disorder.
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