Neurons and glial cells in bipolar disorder: A systematic review of postmortem brain studies of cell number and size

Gigase, Frederieke; Snijders, Gijsje; Boks, Marco P.; Witte, Lot de

doi:10.1016/j.neubiorev.2019.05.027

Cited by 17 publications

(12 citation statements)

References 80 publications

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“…A further study also showed an increase in oligodendrocyte density along with deficits in axonal markers in prefrontal WM in bipolar disorder patients[ 93 ]. In a systematic review of postmortem brain studies in bipolar disorder, Gigase et al [ 94 ] found no difference in either neurons or glial cells and suggested that findings from existing studies should be validated.…”

Section: Myelin Alterations and Oligodendroglial Dysfunction Evidence...mentioning

confidence: 99%

Insights into myelin dysfunction in schizophrenia and bipolar disorder

Valdés-Tovar¹,

Rodríguez-Ramírez²,

Rodríguez-Cárdenas³

et al. 2022

WJP

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Schizophrenia and bipolar disorder are disabling psychiatric disorders with a worldwide prevalence of approximately 1%. Both disorders present chronic and deteriorating prognoses that impose a large burden, not only on patients but also on society and health systems. These mental illnesses share several clinical and neurobiological traits; of these traits, oligodendroglial dysfunction and alterations to white matter (WM) tracts could underlie the disconnection between brain regions related to their symptomatic domains. WM is mainly composed of heavily myelinated axons and glial cells. Myelin internodes are discrete axon-wrapping membrane sheaths formed by oligodendrocyte processes. Myelin ensheathment allows fast and efficient conduction of nerve impulses through the nodes of Ranvier, improving the overall function of neuronal circuits. Rapid and precisely synchronized nerve impulse conduction through fibers that connect distant brain structures is crucial for higher-level functions, such as cognition, memory, mood, and language. Several cellular and subcellular anomalies related to myelin and oligodendrocytes have been found in postmortem samples from patients with schizophrenia or bipolar disorder, and neuroimaging techniques have revealed consistent alterations at the macroscale connectomic level in both disorders. In this work, evidence regarding these multilevel alterations in oligodendrocytes and myelinated tracts is discussed, and the involvement of proteins in key functions of the oligodendroglial lineage, such as oligodendrogenesis and myelination, is highlighted. The molecular components of the axo-myelin unit could be important targets for novel therapeutic approaches to schizophrenia and bipolar disorder.

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Section: Myelin Alterations and Oligodendroglial Dysfunction Evidence...mentioning

confidence: 99%

Insights into myelin dysfunction in schizophrenia and bipolar disorder

Valdés-Tovar¹,

Rodríguez-Ramírez²,

Rodríguez-Cárdenas³

et al. 2022

WJP

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“…According to our knowledge, this is the first prospective study that tries to explore the correlation between S100B serum levels and mood disorders in adolescents and young patients. Based on the findings on glial pathology in mood disorders in adult patients 17 , 18 in our study, we provided some research questions following our hypothesis: (1) there are any differences in baseline serum S100B levels between depressed, hypomanic patients and healthy controls (2) could baseline S100B levels be influenced by clinical factors (severity of depressive and manic symptoms, medication status, family history of psychiatric and affective disorders, or gender) (3) is there a change between baseline S100B concentrations and euthymic state (as well as in a 2-year follow-up) and finally (4) do different baseline S100B levels predict diagnosis change from unipolar to bipolar disorder in young patients.…”

Section: Introductionmentioning

confidence: 99%

Longitudinal assessment of S100B serum levels and clinical factors in youth patients with mood disorders

Rajewska‐Rager

Dmitrzak‐Węglarz

Kapelski

et al. 2021

Sci Rep

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Mood disorders have been discussed as being in relation to glial pathology. S100B is a calcium-binding protein, and a marker of glial dysfunctions. Although alterations in the S100B expression may play a role in various central nervous system diseases, there are no studies on the potential role of S100B in mood disorders in adolescents and young adults . In a prospective two-year follow-up study, peripheral levels of S100B were investigated in 79 adolescent/young adult patients (aged 14–24 years), diagnosed with mood disorders and compared with 31 healthy control subjects. A comprehensive clinical interview was conducted which focused on clinical symptoms and diagnosis change. The diagnosis was established and verified at each control visit. Serum S100B concentrations were determined. We detected: lower S100B levels in medicated patients, compared with those who were drug-free, and healthy controls; higher S100B levels in a depressed group with a family history of affective disorder; correlations between age and medication status; sex-dependent differences in S100B levels; and lack a of correlation between the severity of depressive or hypo/manic symptoms. The results of our study indicate that S100B might be a trait-dependent rather than a state-dependent marker. Due to the lack of such studies in the youth population, further research should be performed. A relatively small sample size, a lack of exact age-matched control group, a high drop-out rate.

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“…Cumulatively, these findings show that the levels of the αisoforms of the Na + , K + -ATPase in the brain differ between BD patients and controls and that the changes vary between different brain regions. It is well established that alterations in both neuronal [40,41] and glial cells [42,43] occur in the brain of BD patients. It is therefore not surprising that we detected alterations in both the α2 and α3 isoforms, which are largely expressed in glial [14] and neuronal cells [15,16], respectively.…”

Section: Discussionmentioning

confidence: 99%

Na+, K+-ATPase α Isoforms and Endogenous Cardiac Steroids in Prefrontal Cortex of Bipolar Patients and Controls

Singh¹,

Федорова

Wei

et al. 2020

IJMS

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Bipolar disorder is a chronic multifactorial psychiatric illness that affects the mood, cognition, and functioning of about 1–2% of the world’s population. Its biological basis is unknown, and its treatment is unsatisfactory. The α1, α2, and α3 isoforms of the Na+, K+-ATPase, an essential membrane transporter, are vital for neuronal and glial function. The enzyme and its regulators, endogenous cardiac steroids like ouabain and marinobufagenin, are implicated in neuropsychiatric disorders, bipolar disorder in particular. Here, we address the hypothesis that the α isoforms of the Na+, K+-ATPase and its regulators are altered in the prefrontal cortex of bipolar disease patients. The α isoforms were determined by Western blot and ouabain and marinobufagenin by specific and sensitive immunoassays. We found that the α2 and α3 isoforms were significantly higher and marinobufagenin levels were significantly lower in the prefrontal cortex of the bipolar disease patients compared with those in the control. A positive correlation was found between the levels of the three α isoforms in all samples and between the α1 isoform and ouabain levels in the controls. These results are in accordance with the notion that the Na+, K+-ATPase-endogenous cardiac steroids system is involved in bipolar disease and suggest that it may be used as a target for drug development.

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Neurons and glial cells in bipolar disorder: A systematic review of postmortem brain studies of cell number and size

Cited by 17 publications

References 80 publications

Insights into myelin dysfunction in schizophrenia and bipolar disorder

Insights into myelin dysfunction in schizophrenia and bipolar disorder

Longitudinal assessment of S100B serum levels and clinical factors in youth patients with mood disorders

Na+, K+-ATPase α Isoforms and Endogenous Cardiac Steroids in Prefrontal Cortex of Bipolar Patients and Controls

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