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12
From Paper: Association between antidepressant use and reduced risk of intubation or death in hospitalized patients with COVID-19: results from an observational study
Authors: Hoertel, Nicolas, et al
Published: Feb 2021
From Paper: Association between antidepressant use and reduced risk of intubation or death in hospitalized patients with COVID-19: results from an observational study
Authors: Hoertel, Nicolas, et al
Published: Feb 2021
A prior meta-analysis showed that antidepressant use in major depressive disorder was associated with reduced plasma levels of several pro-inflammatory mediators, which have been associated with severe COVID-19. Recent studies also suggest that several antidepressants may inhibit acid sphingomyelinase activity, which may prevent the infection of epithelial cells with SARS-CoV-2, and that the SSRI fluoxetine may exert in-vitro antiviral effects on SARS-CoV-2. We examined the potential usefulness of antidepressant use in patients hospitalized for COVID-19 in an observational multicenter retrospective cohort study conducted at AP-HP Greater Paris University hospitals. Of 7230 adults hospitalized for COVID-19, 345 patients (4.8%) received an antidepressant within 48 h of hospital admission. The primary endpoint was a composite of intubation or death. We compared this endpoint between patients who received antidepressants and those who did not in time-to-event analyses adjusted for patient characteristics, clinical and biological markers of disease severity, and other psychotropic medications. The primary analysis was a multivariable Cox model with inverse probability weighting. This analysis showed a significant association between antidepressant use and reduced risk of intubation or death (HR, 0.56; 95% CI, 0.43–0.73, p < 0.001). This association remained significant in multiple sensitivity analyses. Exploratory analyses suggest that this association was also significant for SSRI and non-SSRI antidepressants, and for fluoxetine, paroxetine, escitalopram, venlafaxine, and mirtazapine (all p < 0.05). These results suggest that antidepressant use could be associated with lower risk of death or intubation in patients hospitalized for COVID-19. Double-blind controlled randomized clinical trials of antidepressant medications for COVID-19 are needed.
13
Authors: Kim, Soo-Jeong, et al
Published: Feb 2021
Authors: Kim, Soo-Jeong, et al
Published: Feb 2021
Abstract Background and aims Impulsiveness is an important factor in the pathophysiology of Internet gaming disorder (IGD), and regional brain functions can be different depending on the level of impulsiveness. This study aimed to demonstrate that different brain mechanisms are involved depending on the level of impulsiveness among patients with IGD. Methods Resting-state functional MRI data were obtained from 23 IGD patients with high impulsivity, 27 IGD patients with low impulsivity, and 22 healthy controls, and seed-based functional connectivity was compared among the three groups. The seed regions were the ventromedial prefrontal cortex (vmPFC), dorsolateral prefrontal cortex, nucleus accumbens (NAcc), and amygdala. Results Connectivity of the vmPFC with the left temporo-parietal junction (TPJ) and NAcc-left insula connectivity were significantly decreased in the patients with high impulsivity, compared with the patients with low impulsivity and healthy controls. On the other hand, amygdala-based connectivity with the left inferior frontal gyrus showed decreases in both patient groups, compared with the healthy controls. Conclusion These findings may suggest a potential relationship between impulsivity and deficits in reward-related social cognition processes in patients with IGD. In particular, certain interventions targeted at vmPFC-TPJ connectivity, found to be impulsivity-specific brain connectivity, are likely to help with addiction recovery among impulsive patients with IGD.
36
From Paper: Long runs of homozygosity are associated with Alzheimer’s disease
Published: Feb 2021
From Paper: Long runs of homozygosity are associated with Alzheimer’s disease
Published: Feb 2021
Abstract Long runs of homozygosity (ROH) are contiguous stretches of homozygous genotypes, which are a footprint of inbreeding and recessive inheritance. The presence of recessive loci is suggested for Alzheimer’s disease (AD); however, their search has been poorly assessed to date. To investigate homozygosity in AD, here we performed a fine-scale ROH analysis using 10 independent cohorts of European ancestry (11,919 AD cases and 9181 controls.) We detected an increase of homozygosity in AD cases compared to controls [ β AVROH (CI 95%) = 0.070 (0.037–0.104); P  = 3.91 × 10 −5 ; β FROH (CI95%) = 0.043 (0.009–0.076); P  = 0.013]. ROHs increasing the risk of AD (OR > 1) were significantly overrepresented compared to ROHs increasing protection ( p  < 2.20 × 10 −16 ). A significant ROH association with AD risk was detected upstream the HS3ST1 locus (chr4:11,189,482‒11,305,456), (β (CI 95%) = 1.09 (0.48 ‒ 1.48), p value = 9.03 × 10 −4 ), previously related to AD. Next, to search for recessive candidate variants in ROHs, we constructed a homozygosity map of inbred AD cases extracted from an outbred population and explored ROH regions in whole-exome sequencing data ( N  = 1449). We detected a candidate marker, rs117458494, mapped in the SPON1 locus, which has been previously associated with amyloid metabolism. Here, we provide a research framework to look for recessive variants in AD using outbred populations. Our results showed that AD cases have enriched homozygosity, suggesting that recessive effects may explain a proportion of AD heritability.
6
From Paper: Chronic mild stress-induced protein dysregulations correlated with susceptibility and resiliency to depression or anxiety revealed by quantitative proteomics of the rat prefrontal cortex
Published: Feb 2021
From Paper: Chronic mild stress-induced protein dysregulations correlated with susceptibility and resiliency to depression or anxiety revealed by quantitative proteomics of the rat prefrontal cortex
Published: Feb 2021
Abstract Chronic stress is a significant risk factor for depression as well as anxiety disorders. Yet, the stress-induced specific and common molecular dysregulations of these disorders have not been fully understood. Previously, we constructed a chronic mild stress (CMS) rat model to separate and obtain depression-susceptible, anxiety-susceptible, and insusceptible groups. In this study, the prefrontal cortical proteomes of the three stressed groups were comparatively profiled utilizing isobaric tags for relative and absolute quantitation (iTRAQ)-coupled tandem mass spectrometry approach. A total of 212 protein dysregulations were identified, potentially correlating to susceptibility or resilience to CMS-induced depression or anxiety, and thus might serve as potential protein targets for further investigation. In addition, independent analysis by parallel reaction monitoring identified changes in Gfap, Rhog, Gnai2, Ppp1r1b, and Uqcrh; Tubb6, Urod, Cul1, Spred1, and Gpcpd1; Acadl, Ppp1r1a, Grm2, Mtor, Lsm8, Cplx2, and Tsta3 that were distinctly correlated to depression-susceptible, anxiety-susceptible, or insusceptible groups, respectively. This suggested that identical CMS had different effects on the protein regulation system of the rat prefrontal cortex. Collectively, the present proteomics study of the prefrontal cortex established a significant molecular basis and offered new insights into the specificity and commonality of pathophysiologic mechanisms underlying susceptibility and resiliency to stress-induced depression or anxiety.
7
From Paper: Activation of BDNF by transcription factor Nrf2 contributes to antidepressant-like actions in rodents
Published: Feb 2021
From Paper: Activation of BDNF by transcription factor Nrf2 contributes to antidepressant-like actions in rodents
Published: Feb 2021
Abstract The transcription factor erythroid 2-related factor 2 (Nrf2) and brain-derived neurotrophic factor (BDNF) play a key role in depression. However, the molecular mechanisms underlying the crosstalk between Nrf2 and BDNF in depression remain unclear. We examined whether Nrf2 regulates the transcription of Bdnf by binding to its exon I promoter. Furthermore, the role of Nrf2 and BDNF in the brain regions from mice with depression-like phenotypes was examined. Nrf2 regulated the transcription of Bdnf by binding to its exon I promoter. Activation of Nrf2 by sulforaphane (SFN) showed fast-acting antidepressant-like effects in mice by activating BDNF as well as by inhibiting the expression of its transcriptional repressors (HDAC2, mSin3A, and MeCP2) and revising abnormal synaptic transmission. In contrast, SFN did not affect the protein expression of BDNF and its transcriptional repressor proteins in the medial prefrontal cortex (mPFC) and hippocampus, nor did it reduce depression-like behaviors and abnormal synaptic transmission in Nrf2 knockout mice. In the mouse model of chronic social defeat stress (CSDS), protein levels of Nrf2 and BDNF in the mPFC and hippocampus were lower than those of control and CSDS-resilient mice. In contrast, the protein levels of BDNF transcriptional repressors in the CSDS-susceptible mice were higher than those of control and CSDS-resilient mice. These data suggest that Nrf2 activation increases the expression of Bdnf and decreases the expression of its transcriptional repressors, which result in fast-acting antidepressant-like actions. Furthermore, abnormalities in crosstalk between Nrf2 and BDNF may contribute to the resilience versus susceptibility of mice against CSDS.
7
From Paper: Neuroticism alters the transcriptome of the frontal cortex to contribute to the cognitive decline and onset of Alzheimer’s disease
Published: Feb 2021
From Paper: Neuroticism alters the transcriptome of the frontal cortex to contribute to the cognitive decline and onset of Alzheimer’s disease
Published: Feb 2021
Abstract Accumulating evidence has suggested that the molecular transcriptional mechanism contributes to Alzheimer’s disease (AD) and its endophenotypes of cognitive decline and neuropathological traits, β-amyloid (Aβ) and phosphorylated tangles (TAU). However, it is unknown what is the impact of the AD risk factors, personality characteristics assessed by the NEO Five-Factor Inventory, on the human brain’s transcriptome. Using postmortem human brain samples from 466 subjects, we found that neuroticism has a significant overall impact on the brain transcriptome (omnibus P  = 0.005) but not the other four personality characteristics. Focused on those cognitive decline related gene co-expressed modules, neuroticism has nominally significant associations ( P  < 0.05) with four neuronal modules, which are more related to PHFtau than Aβ across all eight brain regions. Furthermore, the effect of neuroticism on cognitive decline and AD might be mediated through the expression of module 7 and TAU pathology ( P  = 0.008). To conclude, neuroticism has a broad impact on the transcriptome of human brains, and its effect on cognitive decline and AD may be mediated through gene transcription programs related to TAU pathology.
3
Authors: Jog, Mayank. S., et al
Published: Feb 2021
Authors: Jog, Mayank. S., et al
Published: Feb 2021
Abstract Recent clinical trials of transcranial direct current stimulation (tDCS) in depression have shown contrasting results. Consequently, we used in-vivo neuroimaging to confirm targeting and modulation of depression-relevant neural circuitry by tDCS. Depressed participants ( N  = 66, Baseline Hamilton Depression Rating Scale (HDRS) 17-item scores ≥14 and <24) were randomized into Active/Sham and High-definition (HD)/Conventional (Conv) tDCS groups using a double-blind, parallel design, and received tDCS individually targeted at the left dorsolateral prefrontal cortex (DLPFC). In accordance with Ampere’s Law, tDCS currents were hypothesized to induce magnetic fields at the stimulation-target, measured in real-time using dual-echo echo-planar-imaging (DE-EPI) MRI. Additionally, the tDCS treatment trial (consisting of 12 daily 20-min sessions) was hypothesized to induce cerebral blood flow (CBF) changes post-treatment at the DLPFC target and in the reciprocally connected anterior cingulate cortex (ACC), measured using pseudo-continuous arterial spin labeling (pCASL) MRI. Significant tDCS current-induced magnetic fields were observed at the left DLPFC target for both active stimulation montages (Brodmann’s area (BA) 46: p HD  = 0.048, Cohen’s d HD  = 0.73; p Conv  = 0.018, d Conv  = 0.86; BA 9: p HD  = 0.011, d HD  = 0.92; p Conv  = 0.022, d Conv  = 0.83). Significant longitudinal CBF increases were observed (a) at the left DLPFC stimulation-target for both active montages ( p HD  = 3.5E−3, d HD  = 0.98; p Conv  = 2.8E−3, d Conv  = 1.08), and (b) at ACC for the HD-montage only ( p HD  = 2.4E−3, d HD  = 1.06; p Conv  = 0.075, d Conv  = 0.64). These results confirm that tDCS-treatment (a) engages the stimulation-target, and (b) modulates depression-relevant neural circuitry in depressed participants, with stronger network-modulations induced by the HD-montage. Although not primary outcomes, active HD-tDCS showed significant improvements of anhedonia relative to sham, though HDRS scores did not differ significantly between montages post-treatment.
6
From Paper: Young people who purchase loot boxes are more likely to have gambling problems: An online survey of adolescents and young adults living in NSW Australia
Published: Feb 2021
From Paper: Young people who purchase loot boxes are more likely to have gambling problems: An online survey of adolescents and young adults living in NSW Australia
Published: Feb 2021
Abstract Background and aims Loot boxes are a common feature in video games where players win, buy or are gifted a virtual box or other container that is unwrapped to reveal virtual items of value, such as skins, weapons, in-game currency or special abilities. The current study aimed to relate the use of loot boxes to gambling problems and harm. Methods An online survey was conducted with 1,954 adolescents and young adults from NSW Australia, 59.9% female (aged 12–24), recruited by online panel aggregator, Qualtrics. Results Buying and selling loot boxes was associated with higher 12-month gambling frequency and gambling problems in young adults, aged 18–24 (Problem Gambling Severity Index). Young adults who bought loot boxes additionally had more gambling-related harms (Short Gambling Harms Screen). Young women, aged 18–24, who opened, bought and/or sold loot boxes spent more money in the last 12 months on gambling. In adolescents, aged 12–17, buying loot boxes was similarly associated with gambling problems (DSM-IV-MR-J). Furthermore, adolescent girls who bought and/or sold loot boxes viewed gambling more positively than other girls (Attitudes Towards Gambling Scale). There was no evidence, however, that longer-term experience in opening or purchasing loot boxes, a differentiating feature of the survey, is associated with current gambling problems. Discussion and conclusions This study suggests that loot boxes may be attractive to people who are already predisposed to engage in other gambling, and females who use loot boxes may have unique vulnerabilities to gambling problems that could be explored in future research.
2
Authors: Warhaftig, Gal, et al
Published: Feb 2021
Authors: Warhaftig, Gal, et al
Published: Feb 2021
Abstract Post-traumatic-stress-disorder (PTSD) is a stress-related condition that may develop after exposure to a severe trauma-event. One of the core brain areas that is considered to be a key regulatory region of PTSD is the amygdala. Specifically, the central amygdala (CeA) is involved in emotion processing and associative fear learning memory, two main circuits involved in PTSD. Long term dysregulation of trauma-related emotional processing may be caused by neuroadaptations that affect gene expression. The adenosine-(A) to-inosine (I) RNA editing machinery is a post-transcriptional process that converts a genomic encoded A to I and is critical for normal brain function and development. Such editing has the potential to increase the transcriptome diversity, and disruption of this process has been linked to various central nervous system disorders. Here, we employed a unique animal model to examine the possibility that the RNA editing machinery is involved in PTSD. Detection of RNA editing specifically in the CeA revealed changes in the editing pattern of the 5-HT2C serotonin receptor (5-HT2CR) transcript accompanied by dynamic changes in the expression levels of the ADAR family enzymes ( ADAR and ADARb1 ). Deamination by ADAR and ADARb1 enzymes induces conformational changes in the 5-HT2CR that decrease the G-protein-coupling activity, agonist affinity, and thus serotonin signaling. Significantly, a single intra-CeA administration of a 5-HT2CR pharmacological antagonist produced a robust alleviation of PTSD-like behaviors (that was maintained for three weeks) as well as single systemic treatment. This work may suggest the way to a new avenue in the understanding of PTSD regulation.
2
Authors: Anne B. Koopmans, Mario H. Braakman, David J. Vinkers, Hans W. Hoek, Peter N. van Harten
Published: Feb 2021
Authors: Anne B. Koopmans, Mario H. Braakman, David J. Vinkers, Hans W. Hoek, Peter N. van Harten
Published: Feb 2021
Abstract Extensive migration has led to the necessity of knowledge regarding the treatment of migrants with different ethnical backgrounds. This is especially relevant for pharmacological treatment, because of the significant variation between migrant groups in their capacity to metabolize drugs. For psychiatric medications, CYP2D6 and CYP2C19 enzymes are clinically relevant. The aim of this meta-analysis was to analyze studies reporting clinically useful information regarding CYP2D6 and CYP2C19 genotype frequencies, across populations and ethnic groups worldwide. To that end, we conducted a comprehensive meta-analysis using Embase, PubMed, Web of Science, and PsycINFO (>336,000 subjects, 318 reports). A non-normal metabolizer (non-NM) probability estimate was introduced as the equivalent of the sum-prevalence of predicted poor, intermediate, and ultrarapid metabolizer CYP2D6 and CYP2C19 phenotypes. The probability of having a CYP2D6 non-NM predicted phenotype was highest in Algeria (61%) and lowest in Gambia (2.7%) while the probability for CYP2C19 was highest in India (80%) and lowest in countries in the Americas, particularly Mexico (32%). The mean total probability estimates of having a non-NM predicted phenotype worldwide were 36.4% and 61.9% for CYP2D6 and CYP2C19, respectively. We provide detailed tables and world maps summarizing clinically relevant data regarding the prevalence of CYP2D6 and CYP2C19 predicted phenotypes and demonstrating large inter-ethnic differences. Based on the documented probability estimates, pre-emptive pharmacogenetic testing is encouraged for every patient who will undergo therapy with a drug(s) that is metabolized by CYP2D6 and/or CYP2C19 pathways and should be considered in case of treatment resistance or serious side effects.
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