GABAergic dysfunction in schizophrenia and mood disorders as reflected by decreased levels of glutamic acid decarboxylase 65 and 67 kDa and Reelin proteins in cerebellum.
GABAergic dysfunction in schizophrenia and mood disorders as reflected by decreased levels of glutamic acid decarboxylase 65 and 67 kDa and Reelin proteins in cerebellum.
GABAergic dysfunction in schizophrenia and mood disorders as reflected by decreased levels of glutamic acid decarboxylase 65 and 67 kDa and Reelin proteins in cerebellum.
This unexpected result suggests a model that could explain the dual action of VPA in stabilizing mood: we propose that euthymic mood is dependent on stable PIns signaling and that VPA may limit mood swings to mania by decreasing PIns signaling, and that it may limit mood swings to depression by inhibiting PO and thus increasing PIns signaling.
It describes the identification of prolyl oligopeptidase in D. discoideum as a modulator of inositol phosphate signalling, and the subsequent identification of a common mechanism of action of three anti-manic drugs in mammalian neurons.
The 5-HTTLPR polymorphism could be a useful contributor, among other clinical variables, to predict the risk for manic switches when a patient with bipolar disorder is treated with antidepressant drugs.
The association analysis performed showed a significantly higher rate of homozygous s/s genotype for 5-HTTLPR among patients with a history of antidepressant-induced mania (60% patients s/s versus 40% l/l, chi, P=0.04).
Sodium-myo-inositol co-transporter (SMIT-1) mRNA is increased in neutrophils of patients with bipolar 1 disorder and down-regulated under treatment with mood stabilizers.
PEA-BP-I was defined as DSM-IV BP I (manic or mixed phase), with cardinal symptoms (elation and/or grandiosity), to avoid diagnosing mania by symptoms that overlapped with those of ADHD, and by a CGAS score of < or =60.
PEA-BP-I was defined as DSM-IV BP I (manic or mixed phase), with cardinal symptoms (elation and/or grandiosity), to avoid diagnosing mania by symptoms that overlapped with those of ADHD, and by a CGAS score of < or =60.
The continuity/spectrum between BP (mainly BP-II) and MDD was supported by the following findings:(1) high frequency of mixed states (mixed mania, mixed hypomania, mixed depression, i.e. co-occurring depression and noneuphoric manic/hypomanic symptoms) because opposite polarity symptoms in the same episode do not support a hypomania/mania-depression splitting; (2) MDD was the most common mood disorder in BP probands' relatives; (3) no bimodal distribution of distinguishing symptoms between BP and MDD; (4) bipolar signs not uncommon in MDD; (5) many MDD shifting to BP; (6) many lifetime manic/hypomanic symptoms in MDD; (7) correlation between lifetime manic/hypomanic symptoms and MDD symptoms; (8) hypomania factors in MDD; (9) MDD often recurrent; (10) similar cognitive style.