Increased oxidative stress in the mitochondria isolated from lymphocytes of bipolar disorder patients during depressive episodes

Valvassori, Samira S.; Bavaresco, Daniela V.; Cechinel-Recco, Kelen; Steckert, Amanda V.; Varela, Roger B.; Borges, Cenita Pereira; Carvalho-Silva, Milena; Gomes, Lara M.; Streck, Emílio L.; Quevedo, Joao L De

doi:10.1016/j.psychres.2018.03.089

Cited by 46 publications

(25 citation statements)

References 63 publications

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“…20 Several clinical and animal studies have reported alterations in various energetic metabolism components, including downregulation of nuclear mRNA molecules and proteins involved in the Krebs cycle, electron transport chain (ETC) I-IV complexes, and creatine kinase, as well as a marked decrease in the activity of ETC complexes and Krebs cycle enzymes. [130][131][132][133][134][135][136][137][138][139][140][141][142][143] Together, these studies suggest a reduced ability to oxidize NADH and FADH and transfer electrons to ubiquinone in BD, resulting in reactive oxygen species (ROS) production through an increase in the rate of electron leakage by ETC complexes.…”

Section: Mitochondrial Dysfunction and Oxidative Stressmentioning

confidence: 99%

Neurobiology of bipolar disorders: a review of genetic components, signaling pathways, biochemical changes, and neuroimaging findings

Scaini

Valvassori

Diaz

et al. 2020

Braz. J. Psychiatry

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Bipolar disorder (BD) is a chronic mental illness characterized by changes in mood that alternate between mania and hypomania or between depression and mixed states, often associated with functional impairment. Although effective pharmacological and non-pharmacological treatments are available, several patients with BD remain symptomatic. The advance in the understanding of the neurobiology underlying BD could help in the identification of new therapeutic targets as well as biomarkers for early detection, prognosis, and response to treatment in BD. In this review, we discuss genetic, epigenetic, molecular, physiological and neuroimaging findings associated with the neurobiology of BD. Despite the advances in the pathophysiological knowledge of BD, the diagnosis and management of the disease are still essentially clinical. Given the complexity of the brain and the close relationship between environmental exposure and brain function, initiatives that incorporate genetic, epigenetic, molecular, physiological, clinical, environmental data, and brain imaging are necessary to produce information that can be translated into prevention and better outcomes for patients with BD.

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Section: Mitochondrial Dysfunction and Oxidative Stressmentioning

confidence: 99%

Neurobiology of bipolar disorders: a review of genetic components, signaling pathways, biochemical changes, and neuroimaging findings

Scaini

Valvassori

Diaz

et al. 2020

Braz. J. Psychiatry

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“…Several of these mechanisms are implicated with affective disorder etiology including anxiety, [ 33,34 ] depression, [ 35–37 ] PTSD, [ 38 ] anorexia nervosa, [ 39 ] and bipolar disorder. [ 40 ] Among these studies, CRF has been particularly investigated.…”

Section: Mitochondria Are Essential To the Etiology Of Affective Disomentioning

confidence: 99%

Information Processing in Affective Disorders: Did an Ancient Peptide Regulating Intercellular Metabolism Become Co‐Opted for Noxious Stress Sensing?

Lovejoy

Hogg

2020

BioEssays

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Affective disorders arise in stressful situations from aberrant sensory information integration that affects energetic nutrient (i.e., glucose) utilization to the cognitive centers of the brain. Because energy flow is mediated by molecular signals and receptors that evolved before the first complex brains, the phylogenetically oldest signaling systems are essential in the etiology of affective disorders. The corticotropin‐releasing factor (CRF) peptide subfamily is a phylogenetically old metazoan peptide family and is pivotal for regulating organismal energy response associated with stress. Highly conserved, both the CRF peptide family and its receptors possess a structural relationship to the teneurins, and their receptors, latrophilins, respectively. The CRF homologous region of teneurin is defined as the “teneurin C‐terminal associated peptide” (TCAP) and antagonizes CRF action, regulates mitochondrial energy production, and is anxiolytic in vivo. Here, it is postulated that TCAP represents an ancient peptide that mediates intercellular information transfer of stressful and noxious events by regulating energy utilization among neurons.

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“…ROS are mostly generated by mitochondria, which play a key role in meeting cellular energy demands [23]. Importantly, decreases in mitochondrial numbers as well as changes in mitochondria morphology and function have been reported in schizophrenia [6] and BD [24]. In addition, mitochondrial DNA polymorphisms have been associated to increase familial risk for schizophrenia [25].…”

Section: Os In Mood and Psychotic Disordersmentioning

confidence: 99%

Do Immune Dysregulations and Oxidative Damage Drive Mood and Psychotic Disorders?

Morrens¹,

Coppens²,

Walther³

2019

Neuropsychobiology

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Increased oxidative stress in the mitochondria isolated from lymphocytes of bipolar disorder patients during depressive episodes

Cited by 46 publications

References 63 publications

Neurobiology of bipolar disorders: a review of genetic components, signaling pathways, biochemical changes, and neuroimaging findings

Neurobiology of bipolar disorders: a review of genetic components, signaling pathways, biochemical changes, and neuroimaging findings

Information Processing in Affective Disorders: Did an Ancient Peptide Regulating Intercellular Metabolism Become Co‐Opted for Noxious Stress Sensing?

Do Immune Dysregulations and Oxidative Damage Drive Mood and Psychotic Disorders?

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