Immunity, Inflammation, and Bipolar Disorder: Diagnostic and Therapeutic Implications

Hamdani, Nora; Doukhan, Raphaël; Kurtlucan, Ozlem; Tamouza, Ryad; Leboyer, Marion

doi:10.1007/s11920-013-0387-y

Cited by 94 publications

(61 citation statements)

References 79 publications

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“…On the other hand, adiposity and diabetes are associated with an increased risk for depressive mood changes, possibly associated with chronic low-grade inflammation [24,25]. In this context, sICAM-1 elevation might be a common pathogenetic factor for mood disorders and mood changes during metabolic disorders, diabetes, chronic low-grade inflammation as well as vascular complications, and would also support the hypothesis of a subclinical increased permeability of the BBB [26]. Future trials may also assess the relationships adhesion molecule expression with steroid regulation.…”

Section: Discussionmentioning

confidence: 99%

Soluble Intracellular Adhesion Molecule-1 in Patients with Unipolar or Bipolar Affective Disorders: Results from a Pilot Trial

et al. 2016

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Background: Immunological and vascular markers may play a role in the pathophysiology of mood disorders and mood changes. Aim: To test whether the cell adhesion molecule soluble intracellular adhesion molecule-1 (sICAM-1) may serve as a biomarker for patients with unipolar or bipolar affective disorders when compared to a healthy control group, and whether sICAM-1 blood levels change during different mood states. Methods: sICAM-1 serum concentrations were compared between 20 healthy controls and 48 patients with affective disorders (unipolar, bipolar II and bipolar I disorder) during different mood states (euthymic mood state, depression or mania). Results: When compared to healthy controls, patients with affective disorders had significantly higher sICAM-1 levels during the euthymic state (p = 0.015). Differences became more pronounced during depression (p = 0.013). When unipolar and bipolar patients were analyzed separately, unipolar patients significantly differed from controls during the euthymic and depressive mood state, while bipolar II patients showed a trend towards higher sICAM-1 levels during depression. Patients with bipolar I disorders had significantly higher sICAM-1 levels during manic states when compared to controls (p = 0.007). Conclusions: sICAM-1 elevation in unipolar and bipolar patients, independent of mood changes, might support the hypothesis of chronic immune activation and endothelial dysfunction in patients with affective disorders.

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Section: Discussionmentioning

confidence: 99%

Soluble Intracellular Adhesion Molecule-1 in Patients with Unipolar or Bipolar Affective Disorders: Results from a Pilot Trial

et al. 2016

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“…Our early works also found that higher levels of soluble interleukin-2 receptor (sIL-2R) (5,10) and interleukin 1 receptor antagonist (IL-1Ra) (5,11) are accompanied with bipolar mania. Furthermore, the abnormalities of total immunoglobulins levels in body fluid are observed in BD patients (12,13).…”

mentioning

confidence: 99%

Antibody Profiling of Bipolar Disorder Using Escherichia coli Proteome Microarrays

Chen

Syu

Chung

et al. 2015

Molecular & Cellular Proteomics

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To profile plasma antibodies of patients with bipolar disorder (BD), an E. coli proteome microarray comprising ca. 4200 proteins was used to analyze antibody differences between BD patients and mentally healthy controls (HCs). The plasmas of HCs and patients aged 18 -45 years with bipolar I disorder (DSM-IV) in acute mania (BD-A) along with remission (BD-R) were collected. The initial samples consisting of 19 BD-A, 20 BD-R, and 20 HCs were probed with the microarrays. After selecting protein hits that recognized the antibody differences between BD and HC, the proteins were purified to construct BD focus arrays for training diagnosis committees and validation. Additional six BD-A, six BD-R, six HCs, and nine schizophrenic disorder (SZ, as another psychiatric control) samples were individually probed with the BD focus arrays. The trained diagnosis committee in BD-A versus HC combined top six proteins, including rpoA, thrA, flhB, yfcI, ycdU, and ydjL. However, the optimized committees in BD-R versus HC and BD-A versus BD-R were of low accuracy (< 0.6). In the single blind test using another four BD-A, four HC, and four SZ samples, the committee of BD-A versus HC was able to classify BD-A versus HC and SZ with 75% sensitivity and 80% specificity that both HC and SZ were regarded as negative controls. The consensus motif of the six proteins, which form the committee of BD-A versus HC, is [KE]DIL[AG]L[LV]I[NL][IC][SVKH]G[LV][VN][LV] byGapped Local Alignment of Motifs. We demonstrated that the E. coli proteome microarray is capable of screening BD plasma antibody differences and the selected proteins committee was successfully used for BD diagnosis with

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“…These include alterations in the metabolism and action of cholinergic [14], glutaminergic [15], GABAergic [16], and opioid [17] neurotransmission as well as changes in the activity of proteins located at the post-synaptic densities [18]. In addition, strong evidence showed that mitochondrial function [19,20] and oxidative stress [21] and inflammation [22,23] participate in the etiology of BD: Reduced antioxidant capacity was described in bipolar patients, manifested by decreased levels of glutathione in post-mortem prefrontal cortex samples [24]. Downregulation of a number of antioxidant genes, including Superoxide dismutase (SOD1), was found in BD [25].…”

Section: Depressive and Bipolar Disorder (Bd)mentioning

confidence: 99%

Na+, K+-ATPase Signaling and Bipolar Disorder

Lichtstein¹,

Ilani²,

Rosen³

et al. 2018

IJMS

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Bipolar disorder (BD) is a severe and common chronic mental illness characterized by recurrent mood swings between depression and mania. The biological basis of the disease is poorly understood and its treatment is unsatisfactory. Although in past decades the “monoamine hypothesis” has dominated our understanding of both the pathophysiology of depressive disorders and the action of pharmacological treatments, recent studies focus on the involvement of additional neurotransmitters/neuromodulators systems and cellular processes in BD. Here, evidence for the participation of Na+, K+-ATPase and its endogenous regulators, the endogenous cardiac steroids (ECS), in the etiology of BD is reviewed. Proof for the involvement of brain Na+, K+-ATPase and ECS in behavior is summarized and it is hypothesized that ECS-Na+, K+-ATPase-induced activation of intracellular signaling participates in the mechanisms underlying BD. We propose that the activation of ERK, AKT, and NFκB, resulting from ECS-Na+, K+-ATPase interaction, modifies neuronal activity and neurotransmission which, in turn, participate in the regulation of behavior and BD. These observations suggest Na+, K+-ATPase-mediated signaling is a potential target for drug development for the treatment of BD.

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Immunity, Inflammation, and Bipolar Disorder: Diagnostic and Therapeutic Implications

Cited by 94 publications

References 79 publications

Soluble Intracellular Adhesion Molecule-1 in Patients with Unipolar or Bipolar Affective Disorders: Results from a Pilot Trial

Soluble Intracellular Adhesion Molecule-1 in Patients with Unipolar or Bipolar Affective Disorders: Results from a Pilot Trial

Antibody Profiling of Bipolar Disorder Using Escherichia coli Proteome Microarrays

Na+, K+-ATPase Signaling and Bipolar Disorder

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