Disease relevance of Bipolar Disorder

• Amantadine and human Borna disease virus in vitro and in vivo in an infected patient with bipolar depression [1].
• OBJECTIVE: To assess for familial aggregation of fibromyalgia (FM) and measures of tenderness and pain, and for familial coaggregation of FM and major mood disorder (major depressive disorder or bipolar disorder) [2].
• These methods have already been used to reveal the profile of brain anomalies in studies of dementia, epilepsy, depression, childhood- and adult-onset schizophrenia, bipolar disorder, attention-deficit/hyperactivity disorder, fetal alcohol syndrome, Tourette syndrome, Williams syndrome, and in methamphetamine abusers [3].
• The authors used a systematic life-chart methodology to observe four patients with bipolar disorder in whom long periods (6-15 years) of effective lithium prophylaxis were followed by relapses on lithium discontinuation [4].
• Severe psychiatric disorders such as schizophrenia, bipolar disorder and major depressive disorder are brain diseases of unknown origin [5].

Psychiatry related information on Bipolar Disorder

• CONCLUSIONS: We conclude that, like schizophrenic patients, patients with psychotic bipolar disorder have elevations of D2 dopamine receptor Bmax values and that such elevations in affective disorder are more closely associated with the presence of psychosis than with mood abnormality [6].
• Using positron emission tomography, we studied cerebral glucose metabolism in drug-free, age- and sex-matched, right-handed patients with unipolar depression (n = 10), bipolar depression (n = 10), obsessive-compulsive disorder (OCD) with secondary depression (n = 10), OCD without major depression (n = 14), and normal controls (n = 12) [7].
• Disrupted in schizophrenia 1 (DISC1): association with schizophrenia, schizoaffective disorder, and bipolar disorder [8].
• The authors measured RBC/plasma lithium ratios in 33 patients with primary diagnoses of unipolar depression (N=20), bipolar depression (N=9), schizo-affective psychosis (N=2), and alcoholism (N=2) [9].
• Moreover, when overlapping ADHD symptoms were subtracted, on average, 79% maintained their diagnosis of major depression, 56% maintained their diagnosis of bipolar disorder, and 75% maintained their diagnosis of generalized anxiety disorder [10].

High impact information on Bipolar Disorder

• Genetic mapping using haplotype, association and linkage methods suggests a locus for severe bipolar disorder (BPI) at 18q22-q23 [11].
• Serum lithium during treatment of bipolar disorder [12].
• Inositol monophosphatase--a putative target for Li+ in the treatment of bipolar disorder [13].
• However, inhibitors of IMPase mimic the effects of Li+ on some aspects of PI cell signalling, thus highlighting the potential of IMPase as a target for the treatment of bipolar disorder [13].
• We propose that modulation of brain PACAP signaling might represent a new opportunity in the treatment of bipolar disorder [14].

Chemical compound and disease context of Bipolar Disorder

• Thyrotropin-releasing-hormone test in unipolar and bipolar depression [15].
• Bipolar affective psychosis after vigabatrin [16].
• Reduction of vanadate, a possible explanation of the effect of phenothiazines in manic-depressive psychosis [17].
• The results of this study indicate the potential clinical utility of the anticonvulsant mood stabilizer, valproate, in bipolar disorder with co-occurring alcohol dependence [18].
• The results indicate that lamotrigine is an effective, well-tolerated maintenance treatment for bipolar disorder, particularly for prophylaxis of depression [19].
• Within the hippocampus, abnormalities of the ionotropic glutamate receptors were found in bipolar disorder with metabotropic glutamate receptors being relatively understudied [20].

Biological context of Bipolar Disorder

• We evaluated the immunoreactivity of the regulatory and catalytic subunits of cAMP-dependent protein kinase (protein kinase A) and 1 of its substrates, Rap1, in platelets from untreated euthymic, manic, and depressed patients with bipolar disorder and healthy subjects [21].
• This finding suggests that natural variations in GR gene expression can contribute to the fine-tuning of emotional stability or lability and may play a role in bipolar disorder [22].
• Mutation analysis of SYNJ1: a possible candidate gene for chromosome 21q22-linked bipolar disorder [23].
• Two of the eight new SNPs, one in intron 8 and one in intron 13, were found to be moderately associated with bipolar disorder, each in one of the two independent samples [24].
• METHOD: The prepubertal and early adolescent bipolar disorder phenotype was defined as current DSM-IV bipolar I disorder (manic or mixed phase) with at least one cardinal mania criterion (i.e., euphoria and/or grandiosity) to ensure differentiation from attention deficit hyperactivity disorder [25].

Anatomical context of Bipolar Disorder

• CONCLUSIONS: The density of gamma-aminobutyric acid interneurons that express the NMDA NR(2A)subunit appears to be decreased in schizophrenia and bipolar disorder [26].
• OBJECTIVE: This investigation evaluated the relationship between changes in thyroid indices and mood stability during lithium and carbamazepine prophylaxis for bipolar disorder [27].
• Reduction of synapsin in the hippocampus of patients with bipolar disorder and schizophrenia [28].
• Together, these studies support a model of bipolar disorder that involves dysfunction within subcortical (striatal-thalamic)-prefrontal networks and the associated limbic modulating regions (amygdala, midline cerebellum) [29].
• Inositol monophosphatase in immortalized lymphoblastoid cell lines indicates susceptibility to bipolar disorder and response to lithium therapy [30].

Gene context of Bipolar Disorder

• Here we performed a biochemical analysis of DISC1 protein in a well characterized set of autopsied brains, including brains of patients with SZ, bipolar disorder, and major depression (MD), as well as normal control brains [31].
• Recent biochemical data, however, indicate that CB also has characteristics of a Ca(2+) sensor and activates myo-inositol monophosphatase (IMPase), a key enzyme of the inositol-1,4,5-trisphosphate signaling cascade and an assumed target of mood-stabilizing drugs in the treatment of bipolar disorder [32].
• RESULTS: Relative to the comparison subjects, subjects with bipolar disorder without panic disorder, but not those with comorbid bipolar disorder and panic disorder, showed significantly higher frequencies of the COMT Met158 and the short 5-HTTLPR alleles and genotypes [33].
• Family-based association study of 76 candidate genes in bipolar disorder: BDNF is a potential risk locus. Brain-derived neutrophic factor [34].
• Together, these data are consistent with the presence of multiple variants in DAT1 that convey susceptibility to bipolar disorder [24].
• Growth factor gene cascades in Bipolar disorder [35]
• Oligodendrocytes and genes in Bipolar disorder [36]
• Genes   and environmental risk factors   implicated in Bipolar disorder

Analytical, diagnostic and therapeutic context of Bipolar Disorder

• Long-term lithium therapy for bipolar disorder: systematic review and meta-analysis of randomized controlled trials [37].
• In the present study, the secreted isoform of N-CAM (SEC N-CAM), synaptophysin, and actin proteins were measured in the hippocampus of controls, suicide victims, and patients with bipolar disorder or schizophrenia by quantitative Western immunoblotting [38].
• CONCLUSIONS: The high rates of response to tranylcypromine in both the initial and crossover double-blind studies document the efficacy of MAOI treatment for anergic bipolar depression [39].
• This index contributed a unique risk for suicide after the authors controlled for age, psychiatric hospitalization, suicide attempts, bipolar disorder, major depressive disorder, and unemployment status [40].
• Treatment of imipramine-resistant recurrent depression, IV: A double-blind crossover study of tranylcypromine for anergic bipolar depression [39].

References