By comparing the differences between the three groups, we obtained the following results: (1) both the BD and MDD patients showed shared weaker intra-network FC in the left mPFC and right precuneus within the DMN as well as weaker inter-ROI FC between the left AI and right AI compared with the healthy controls; (2) the BD had weaker while the MDD had stronger intra-network FC in the right dlPFC within the rCEN as well as stronger inter-ROI FC between the right dlPFC and right ANG compared with the healthy controls; (3) the BD showed specific, stronger inter-ROI FC between the left PPC and right AI as well as stronger inter-network FC between the lCEN and SN compared with either the MDD or the control group.
Using mature miRNA profiling and quantitative real-time PCR (qRT-PCR) in the orbitofrontal cortex (OFC) of SCZ (N = 29; 20 male and 9 female), BD (N = 26; 12 male and 14 female), and unaffected control (N = 25; 21 male and 4 female) subjects, we uncovered that miR-223, an exosome-secreted miRNA that targets glutamate receptors, was increased at the mature miRNA level in the OFC of SCZ and BD patients with positive history of psychosis at the time of death and was inversely associated with deficits in the expression of its targets glutamate ionotropic receptor NMDA-type subunit 2B (GRIN2B) and glutamate ionotropic receptor AMPA-type subunit 2 (GRIA2).
PEDF levels were especially lower in MDD patients than in HCs and patients with bipolar disorder (BD) and schizophrenia (SCZ), and elevated PEDF were consistent with decreased HAM-D scores in patients given antidepressant therapy (ADT).
Twenty-three patients with BD and 23 controls underwent retinal evaluation using SS deep range imaging (DRI) Triton OCT. Full retinal thickness, the ganglion cell layer (GCL), the retinal nerve fiber layer (RNFL), and choroidal thickness were evaluated with automated segmentation software.
After adjustment for age, sex, socioeconomic status, region of residence, and year, there was a higher incidence in the IBD cohort compared with controls for depression (incidence rate ratio [IRR], 1.58; 95% confidence interval [CI], 1.41-1.76), anxiety disorder (IRR, 1.39; 95% CI, 1.26-1.53), bipolar disorder (IRR, 1.82; 95% CI, 1.44-2.30), and schizophrenia (IRR, 1.64; 95% CI, 0.95-2.84).
Offspring (ages 8-17) of parents with BD (OBP, n = 32), offspring of comparison parents with non-BD psychopathology (OCP, n = 30), and offspring of healthy parents (OHP, n = 24) underwent diffusion tensor and functional magnetic resonance imaging while performing an emotional face processing task.
Varying levels of evidence support their roles in neurocognitive disorders (KCTD3), neurodevelopmental disease (KCTD7), bipolar disorder (KCTD12), autism and schizophrenia (KCTD13), movement disorders (KCTD17), cancer (KCTD11), and obesity (KCTD15).
Together, vulnerability to mania-like behavior following d-AMPH challenge and extensive neurotrophic alterations, suggest amphetamine-induced behavioral sensitization is a good model of BD pathophysiology.
The second aim was to investigate possible interaction between the previously published common risk gene variants of ADHD in the ADGRL3 (=LPHN3) gene (rs2305339, rs1397548, rs734644, rs1397547, rs2271338, rs6551665, and rs2345039) and shared risk gene variants of aADHD and BD in the DGKH gene (DGKH rs994856/rs9525580/rs9525584 GAT haplotype) and pre-, peri-, and postnatal risk factors in comparison to a healthy control group.
While implication with BD is novel, COPS2, EID1, and SHC4 are known to be relevant for neuronal differentiation and function and DTWD1 for psychopharmacological side effects.
Targeted and untargeted lipidomic analyses were performed according to GLP guidelines in 67 patients with unipolar or bipolar disorders (20-67 years, 36 male, 31 female) and 405 healthy controls (18-79 years, 142 m, 263 f), who were matched according to gender, age and body mass index.
In the current study, we evaluated expression levels of six apoptosis-related lncRNAs (CCAT2, TUG1, PANDA, NEAT1, FAS-AS1 and OIP5-AS1) in the peripheral blood of bipolar disorder (BD) patients and healthy subjects to assess their contribution in the pathogenesis of BD.
Complex I (NADH dehydrogenase, NDU) and complex IV (cytochrome-c-oxidase, COX) of the mitochondrial electron transport chain have been implicated in the pathophysiology of major psychiatric disorders, such as major depressive disorder (MDD), bipolar disorder (BD), and schizophrenia (SZ), as well as in neurodegenerative disorders, such as Alzheimer disease (AD) and Parkinson disease (PD).
Loss of brain laterality in SCZ and BD corresponds to aberrant epigenetic regulation of TGFB2 and changes in TGFβ signaling, indicating potential avenues for disease prevention/treatment.
Complex I (NADH dehydrogenase, NDU) and complex IV (cytochrome-c-oxidase, COX) of the mitochondrial electron transport chain have been implicated in the pathophysiology of major psychiatric disorders, such as major depressive disorder (MDD), bipolar disorder (BD), and schizophrenia (SZ), as well as in neurodegenerative disorders, such as Alzheimer disease (AD) and Parkinson disease (PD).
Targeted and untargeted lipidomic analyses were performed according to GLP guidelines in 67 patients with unipolar or bipolar disorders (20-67 years, 36 male, 31 female) and 405 healthy controls (18-79 years, 142 m, 263 f), who were matched according to gender, age and body mass index.