"Hence, we aimed to better investigate the involvement of the VGF peptides in schizophrenia by studying their localization in the brain regions relevant for the disease, and revealing their possible modulations in response to certain neuronal alterations occurring in schizophrenia".
>35% of patients with CMCs alone or CMCs and schizophrenia had prescriptions provided by 3 or more PCP providers, which increased to 49.1% for patients with CMCs and depression.
>35% of patients with CMCs alone or CMCs and schizophrenia had prescriptions provided by 3 or more PCP providers, which increased to 49.1% for patients with CMCs and depression.
>35% of patients with CMCs alone or CMCs and schizophrenia had prescriptions provided by 3 or more PCP providers, which increased to 49.1% for patients with CMCs and depression.
<b>Aim:</b> The authors aimed to study cognitive-enhancement- and neuroprotective-effects of Brahmi on novel object recognition memory and GABAergic neuronal density, defined by the presence of calcium binding proteins (CBPs; calbindin (CB), parvalbumin (PV), and calretinin (CR)) in a sub-chronic (2 mg/kg, Bid, ip) phencyclidine (PCP) rat model of schizophrenia.
<b>Aim:</b> The authors aimed to study cognitive-enhancement- and neuroprotective-effects of Brahmi on novel object recognition memory and GABAergic neuronal density, defined by the presence of calcium binding proteins (CBPs; calbindin (CB), parvalbumin (PV), and calretinin (CR)) in a sub-chronic (2 mg/kg, Bid, ip) phencyclidine (PCP) rat model of schizophrenia.
<b>Aim:</b> The authors aimed to study cognitive-enhancement- and neuroprotective-effects of Brahmi on novel object recognition memory and GABAergic neuronal density, defined by the presence of calcium binding proteins (CBPs; calbindin (CB), parvalbumin (PV), and calretinin (CR)) in a sub-chronic (2 mg/kg, Bid, ip) phencyclidine (PCP) rat model of schizophrenia.
<b>Background</b>Brief cognitive-behavioural therapy (CBT) is an emerging treatment for schizophrenia in community settings; however, further trials are needed, especially in non-Western countries.<b>Aims</b>To test the effects of brief CBT for Chinese patients with schizophrenia in the community (trial registration: ChiCTR-TRC-13003709).<b>Method</b>A total of 220 patients with schizophrenia from four districts of Beijing were randomly assigned to either brief CBT plus treatment as usual (TAU) or TAU alone.
<b>Background:</b> Evidence supports that the hypofunction of <i>N</i>-methyl-D-aspartate receptor (NMDAR) and downregulation of disrupted-in-schizophrenia 1 (DISC1) contribute to the pathophysiology of schizophrenia.
<b>Background:</b> Several studies have revealed significant associations between single nucleotide polymorphisms (SNPs) in the cannabinoid receptor 1 (<i>CNR1</i>) gene and a broad spectrum of psychiatric disorders such as major depressive disorder (MDD), attention deficit hyperactivity disorder (ADHD), and schizophrenia.
<b>Conclusion:</b> To our knowledge this is the first study to unpick the influence of <i>DISC1</i> variations on spontaneous neuronal activity in SCZ; Given the emerging evidence that ReHo is a stable inheritable phenotype for schizophrenia, our findings suggest the DISC1 variations are possibly an inheritable source for the altered ReHo in this disorder.
<b>Data Sources:</b> MEDLINE, Google Scholar, Cochrane Database and PsycINFO databases were searched for articles containing all the following exploded MESH terms: schizophrenia [AND] antipsychotic agents/neuroleptics [AND] (weight gain [OR] lipids [OR] insulin [OR] leptin) [AND] treatment outcome.
<b>Discussion:</b> Findings from the VIA 7 study revealed large variations across domains between children born to parents with schizophrenia, bipolar and controls, respectively.
<b>Methods:</b> In planned secondary analyses of a 3 months, double-blind, randomized, placebo-controlled trial (<i>n</i> = 45), we explored effects of the GLP-1 receptor agonist exenatide 2 mg once-weekly (<i>n</i> = 23), or placebo (<i>n</i> = 22) on bone turnover markers (BTMs) and BMD in chronic, obese, antipsychotic-treated patients with schizophrenia spectrum disorder.
<b>Results:</b> Compared to controls, SZ subjects had nonsignificant trends toward a decrease in vGLUT1, and an increase in both vGLUT2 and GAD67. vGLUT1 was negatively correlated with GAD67 in normal controls (NCs) and positively correlated in SZ subjects.
<b>Results:</b> Compared to controls, SZ subjects had nonsignificant trends toward a decrease in vGLUT1, and an increase in both vGLUT2 and GAD67. vGLUT1 was negatively correlated with GAD67 in normal controls (NCs) and positively correlated in SZ subjects.
<b>Results:</b> Compared to controls, SZ subjects had nonsignificant trends toward a decrease in vGLUT1, and an increase in both vGLUT2 and GAD67. vGLUT1 was negatively correlated with GAD67 in normal controls (NCs) and positively correlated in SZ subjects.
<b>Results:</b> Compared with the HC, peripheral IL-10 levels were higher and a significant reduction of FA and AD, and increase of RD and MD were observed in SZ (corrected <i>p</i> < 0.05).
<i>In Silico</i>Model-driven Assessment of the Effects of Brain-derived Neurotrophic Factor Deficiency on Glutamate and Gamma-Aminobutyric Acid: Implications for Understanding Schizophrenia Pathophysiology.
(1)H NMR spectroscopy-based metabonomic analysis was employed to investigate plasma samples from 21 pairs of monozygotic twins discordant for schizophrenia and 8 pairs of age-matched healthy twins in an effort to disentangle genetic and epigenetic components of schizophrenia.
(2) Underexpression of RGS4 in DLPFC is pathophysiologically significant because DLPFC pathology in schizophrenia has been supported by neurocognitive,(3,4) structural(5) and functional(6,7) imaging, postmortem,(8) cellular(9,10) and molecular(11) pathological studies.
(2) We examined the association of three polymorphisms in the 5-HT2A receptor gene (HTR2A) with TD susceptibility--T102C(3) and his452tyr(4) in the coding region and A-1438G(5) in the promoter--in matched schizophrenia patients with (n = 59, SCZ-TD-Y) and without TD (n = 62, SCZ-TD-N) and normal control subjects (n = 96).