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Published By S. Karger Ag

1423-0224, 0302-282x

2022 ◽  
pp. 1-11
Author(s):  
Kasumi Yasuda ◽  
Shinichi Yamada ◽  
Shinya Uenishi ◽  
Natsuko Ikeda ◽  
Atsushi Tamaki ◽  
...  

<b><i>Introduction:</i></b> The hippocampus is relevant to cognitive function in schizophrenia (SCZ) and mood disorder patients. Although not anatomically uniform, it is clearly divided into subfields. This study aimed to elucidate the relationship between hippocampal subfield volume and cognitive function in patients with SCZ, bipolar disorder (BP), and major depressive disorder (MDD). <b><i>Methods:</i></b> The study included 21 patients with SCZ, 22 with BP, and 21 with MDD and 25 healthy controls (HCs). Neurocognitive function was assessed using the Brief Assessment of Cognition in Schizophrenia. We obtained hippocampal subfield volumes using FreeSurfer 6.0. We compared the volumes of the hippocampal subfield between the 4 groups and ascertained correlation between the cognitive composite score and hippocampal subfield volume in each group. <b><i>Results:</i></b> The SCZ group had significantly lower cognitive composite score than the BP, MDD, and HC groups. In the SCZ group, the left and right hippocampus-amygdala transition area and right subiculum and right presubiculum volumes were significantly reduced compared to those in the HC group. The left presubiculum volumes in the SCZ group were significantly reduced compared to those in the MDD group. Subfield volumes did not significantly differ between the BP, MDD, and HC groups. Interestingly, in the SCZ group, volumes of the right CA1, right molecular layer of the hippocampus, and right granule cell and molecular layer of the dentate gyrus were significantly correlated with the cognitive composite score. <b><i>Conclusion:</i></b> Patients with SCZ had poorer cognitive function, which is related to their hippocampal pathology, than those with mood disorders.


2022 ◽  
pp. 1-12
Author(s):  
Tayllon dos Anjos-Garcia ◽  
Alexandre Kanashiro ◽  
Alline Cristina de Campos ◽  
Norberto Cysne Coimbra

<b><i>Introduction:</i></b> Environmental enrichment (EE) is a useful and sophisticated tool that improves rodents’ well-being by stimulating social behaviour and cognitive, motor, and sensory functions. Exposure to EE induces neuroplasticity in different brain areas, including the limbic system, which has been implicated in the control of anxiety and fear. However, the effects of EE on ethologically relevant naturalistic behaviours, such as those displayed by prey in the presence of predators, remain largely unexplored. <b><i>Material and Methods:</i></b> In the present study, we investigated anxiety- and panic attack-like behaviours in a predator (cat)-prey confrontation paradigm and compared them with those in classical assays, such as the elevated plus-maze (EPM), marble-burying, and open field tests (OFTs), using C57BL/6J male mice housed in enriched or standard environments for 6 weeks. <b><i>Results:</i></b> We observed that EE exposure caused enhancement of the levels of anxiety-like behaviours in the EPM and OFTs, increasing risk assessment (an anxiety-related response), and decreasing escape (a panic attack-like response) behaviours during exposure to the predator versus prey confrontation paradigm. <b><i>Conclusion:</i></b> Taken together, our findings suggest that enriched external environments can modify the processing of fear- and anxiety-related stimuli in dangerous situations, changing the decision-making defensive strategy.


2022 ◽  
pp. 1-9
Author(s):  
Qi Wang ◽  
Hongsheng Bi ◽  
Hongfei Huang ◽  
Yitong Wang ◽  
Lili Gong ◽  
...  

<b><i>Background:</i></b> The precise physiological mechanisms of acupuncture in the treatment of depression are still unknown. This study aimed to observe the effects of electroacupuncture (EA) on depression-like behavior of mouse in chronic mild stress (CMS) model and explore the underlying mechanism. <b><i>Methods:</i></b> The depression model was established by using CMS method for 6 weeks. After the third week of the CMS paradigm, EA treatment was performed daily for 15 min over a period of 3 weeks. The antidepressant-like effects of EA were evaluated using the sucrose preference test and the forced swimming test (FST). The protein levels of the nuclear factor-kappa B (NF-κB), p-NF-κB, inhibitor of NF-κB, p-IκBα, NOD-like receptor protein 3, interleukin (IL)-6, IL-1β, IL-18, and tumor necrosis factor-α (TNF-α) in hippocampus of mice were detected. <b><i>Results:</i></b> Sucrose preference was decreased after 6 weeks of CMS and the effects of CMS was reversed by EA. CMS increased immobility time and decreased latency to the first immobility in the FST test, but these effects were reversed by EA. CMS-induced nuclear entry of NF-κB (nuclear/cytoplasmic ratio of NF-κB) with an increase in protein levels of p-NF-κB and p-IκBα in the hippocampus. The CMS also increased NLRP3 levels in the hippocampus. However, these effects were reversed by EA. In addition, the levels of IL-6, IL-1β, IL-18, and TNF-α in the hippocampus were increased by CMS, and these effects of stress were reversed by EA. <b><i>Conclusion:</i></b> EA prevented CMS-induced depressive-like behaviors by inhibiting NF-κB/NLRP3 inflammatory pathway.


2022 ◽  
pp. 1-10
Author(s):  
Gianna Spitta ◽  
Tobias Gleich ◽  
Kristin Zacharias ◽  
Oisin Butler ◽  
Ralph Buchert ◽  
...  

<b><i>Introduction:</i></b> Reduced striatal dopamine D2/3 receptor availability in alcohol use disorder (AUD) has been demonstrated in recent clinical studies and meta-analyses. However, only a limited number of studies investigated extrastriatal D2/3 availability in AUD or in at-risk populations. In line with a dimensional understanding of addiction, extrastriatal dopaminergic neuroadaptations have been suggested to be relevant from a pathobiological perspective. <b><i>Methods:</i></b> We investigated D2/3 receptor availability via <sup>18</sup>F-fallypride positron emission tomography applying a region of interest (ROI) approach. We selected ROIs for the prefrontal cortex (PFC) and the anterior cingulate cortex (ACC). Our sample included 19 healthy controls (low risk [LR]), 19 individuals at high risk (HR) to develop addiction, and 20 recently detoxified AUD patients. <b><i>Results:</i></b> We found significantly higher D2/3 receptor availability of HR compared to AUD in the left and right rostral ACC (rACC), as well as in the left ventrolateral PFC (vlPFC). We did not observe a significant difference between AUD and LR. After corrections for multiple comparisons none of the ROIs reached significance throughout the group comparison. The D2/3 receptor availability in the left rACC was inversely correlated with symptom severity assessed with the Alcohol Dependency Scale. <b><i>Discussion:</i></b> To our knowledge, the present work is the first study investigating extrastriatal D2/3 receptor availabilities in individuals at HR and patients with AUD. The observation that D2/3 receptor availabilities are highest in HR might suggest that their pathobiology differs from subjects with AUD. Future studies are necessary to clarify the intraindividual course of this biomarker over different disease stages and its possible role as a risk or protective factor.


2022 ◽  
pp. 1-10
Author(s):  
Else Refsgaard ◽  
Anne Vibeke Schmedes ◽  
Klaus Martiny

<b><i>Introduction:</i></b> The hypothalamic-pituitary-adrenal axis function in depression has been the subject of considerable interest, and its function has been tested with a variety of methods. We investigated associations between saliva cortisol at awakening and the 24-h urine cortisol output, both measured at study baseline, with endpoint depression scores. <b><i>Methods:</i></b> Patients were admitted to a psychiatric inpatient ward with a major depressive episode and were started on fixed duloxetine treatment. They delivered saliva samples at awakening and 15, 30, and 60 min post-awakening and sampled urine for 24 h. Subsequently, they started a daily exercise program maintained for a 9-week period. Clinician-rated depression severity was blindly assessed with the Hamilton Depression Rating 6-item subscale (HAM-D<sub>6</sub>). The cortisol awakening response was quantified by the area under the curve with respect to the ground (AUC<sub>G</sub>) and with respect to the rise (AUC<sub>I</sub>) using saliva cortisol levels in the 1-h period after awakening. Analysis of expected associations between depression severity, AUC<sub>G</sub>, AUC<sub>I</sub>, exercise, and 24-h cortisol output was performed in a general linear model. <b><i>Results:</i></b> In all, 35 participants delivered saliva or 24-h urine samples. The mean age was 49.0 years (SD = 11.0) with 48.6% females with a mean baseline HAM-D<sub>6</sub> score of 12.2 (SD = 2.3). In a statistical model investigating the association between HAM-D<sub>6</sub> at week 9 as a dependent variable and AUC<sub>I</sub>, concurrent HAM-D<sub>6</sub>, gender, smoking, and exercise volume as covariates, we found a significant effect of AUC<sub>I</sub>, concurrent HAM-D<sub>6</sub>, and exercise. The following statistics were found: AUC<sub>I</sub> (regression coefficient 0.008; <i>F</i> value = 9.1; <i>p</i> = 0.007), concurrent HAM-D<sub>6</sub> (regression coefficient 0.70; <i>F</i> value = 8.0; <i>p</i> = 0.01), and exercise (regression coefficient −0.005; <i>F</i> value = 5.7; <i>p</i> = 0.03). The model had an <i>R</i><sup>2</sup> of 0.43. The association between HAM-D<sub>6</sub> endpoint scores and the AUC<sub>I</sub> showed that higher AUC<sub>I</sub> values predicted higher HAM-D<sub>6</sub> endpoint values. The association between HAM-D<sub>6</sub> endpoint scores and the exercise level showed that a high exercise level was associated with lower HAM-D<sub>6</sub> endpoint values. <b><i>Conclusion:</i></b> The results thus showed that high AUC<sub>I</sub> values predicted less improvement of depression and high exercise levels predicted more improvement of depression. These findings need to be confirmed in larger samples to test if more covariates can improve prediction of depression severity.


2022 ◽  
pp. 1-12
Author(s):  
Amir Keshavarzi ◽  
Aziz Sharifi ◽  
Leila Jahangard ◽  
Alireza Soltanian ◽  
Annette Beatrix Brühl ◽  
...  

<b><i>Background:</i></b> Levetiracetam is an anticonvulsant with a low side effect profile and favorable properties for individuals with bipolar I disorder during their manic phase. Despite initial promising results until about 2008, it appears that this track of research has not been followed-up. To counter this, we tested the influence of adjuvant levetiracetam on acute mania, compared to placebo. More specifically, we performed a randomized, double-blind, placebo-controlled clinical trial among inpatients with bipolar disorder I during their acute phase of mania. <b><i>Methods:</i></b> A total of 72 inpatients (mean age: 33.98 years; 23.6% females) with diagnosed bipolar disorder I and during their acute manic phase were randomly assigned either to the adjuvant levetiracetam (250 mg to a maximum of 1,500 mg) or to the placebo condition. Standard medication was lithium at therapeutic dosages. At baseline, participants completed a series of self-rating questionnaires covering sociodemographic information and subjective sleep. Subjective sleep was re-assessed 24 days later at the end of the study. Experts rated participants’ acute state of mania with the Young Mania Rating Scale at baseline and at day 12 and day 24. Participants’ cognitive performance was assessed at baseline and at day 24 at the end of the study. <b><i>Results:</i></b> Over time, mania scores significantly decreased (large effect size), but more so in the levetiracetam condition, compared to the placebo condition (medium effect size). Likewise, over time, subjective sleep improved (large effect size), but more so in the levetiracetam condition, compared to the placebo condition (large effect size). Over time, cognitive performance improved (large effect size), irrespective of the study condition. <b><i>Conclusions:</i></b> Compared to placebo, adjuvant levetiracetam to lithium improved symptoms of mania, as rated by experts, and subjective sleep quality. Adjuvant levetiracetam had no further favorable (or detrimental) impact on cognitive performance.


2021 ◽  
pp. 1-8
Author(s):  
Kaat Hebbrecht ◽  
Manuel Morrens ◽  
Erik J. Giltay ◽  
Alexander L.N. van Nuijs ◽  
Bernard Sabbe ◽  
...  

<b><i>Introduction:</i></b> Chronic low-grade inflammation is suggested to play a pathophysiological role in bipolar disorder (BD) and its related cognitive dysfunctions. Although kynurenine (KYN) pathway metabolites are key inflammatory mediators, studies investigating the association between KYN metabolism and cognition in BD are scarce. We aimed to explore the relationship between KYN metabolism and cognitive functioning across different mood states in BD. <b><i>Methods:</i></b> Sixty-seven patients with BD (35 depressed and 32 [hypo] manic) and 29 healthy controls were included. Cognitive functioning was assessed at 3 time intervals (baseline, 4, and 8 months) assessing processing speed, sustained attention, verbal memory, working memory, and response inhibition. Plasma samples for quantification of 3-hydroxykynurenine, quinolinic acid, and kynurenic acid (KYNA) were concurrently provided. Linear mixed models were used for statistical analysis. <b><i>Results:</i></b> The manic group showed deficits in all assessed cognitive domains with the exception of verbal memory at all test moments. The bipolar depression group showed deficits in the processing speed at all test moments. Throughout the whole follow-up period, KYNA was significantly lower in both patient groups than in controls. Only in the bipolar depression group, low KYNA was associated with worse global cognitive functioning (<i>B</i> = 0.114, <i>p</i> = 0.02) and slower processing speed in particular (<i>B</i> = 0.139, <i>p</i> = 0.03). <b><i>Conclusion:</i></b> Only in the bipolar depression group, lower KYNA was associated with worse cognitive functioning. Future large-scale longitudinal studies are warranted to confirm the role of KYN metabolites in cognitive impairment in patients with BD and the possible therapeutic implications of this relationship.


2021 ◽  
pp. 1-14
Author(s):  
Claudia Cornelis ◽  
Livia J. De Picker ◽  
Violette Coppens ◽  
Anne Morsel ◽  
Maarten Timmers ◽  
...  

<b><i>Background:</i></b> The “cognitive dysmetria hypothesis” of schizophrenia proposes a disrupted communication between the cerebellum and cerebral cortex, resulting in sensorimotor and cognitive symptoms. Sensorimotor adaptation relies strongly on the function of the cerebellum. <b><i>Objectives:</i></b> This study investigated whether sensorimotor adaptation is reduced in schizophrenia compared with age-matched and elderly healthy controls. <b><i>Methods:</i></b> Twenty-nine stably treated patients with schizophrenia, 30 age-matched, and 30 elderly controls were tested in three motor adaptation tasks in which visual movement feedback was unexpectedly altered. In the “rotation adaptation task” the perturbation consisted of a rotation (30° clockwise), in the “gain adaptation task” the extent of the movement feedback was reduced (by a factor of 0.7) and in the “vertical reversal task,” up- and downward pen movements were reversed by 180°. <b><i>Results:</i></b> Patients with schizophrenia adapted to the perturbations, but their movement times and errors were substantially larger than controls. Unexpectedly, the magnitude of adaptation was significantly smaller in schizophrenia than elderly participants. The impairment already occurred during the first adaptation trials, pointing to a decline in explicit strategy use. Additionally, post-adaptation aftereffects provided strong evidence for impaired implicit adaptation learning. Both negative and positive schizophrenia symptom severities were correlated with indices of the amount of adaptation and its aftereffects. <b><i>Conclusions:</i></b> Both explicit and implicit components of sensorimotor adaptation learning were reduced in patients with schizophrenia, adding to the evidence for a role of the cerebellum in the pathophysiology of schizophrenia. Elderly individuals outperformed schizophrenia patients in the adaptation learning tasks.


2021 ◽  
pp. 1-13
Author(s):  
Mohammadali Amini ◽  
Zohreh Abdolmaleki

<b><i>Introduction:</i></b> Using nanoparticle (NP) drugs can have better effects on the target tissue in various diseases. Alzheimer’s disease (AD) is one of the degenerative neurological diseases that due to its high prevalence, requires the use of more appropriate treatments. Therefore, the aim of this study was consideration of the effect of cannabidiol (CBD) coated by nano-chitosan on learning and memory, hippocampal cannabinoid receptor type 1 (CB1) and cannabinoid receptor type 1 (CB2) levels, and amyloid plaques in an AD rat model. <b><i>Material and Methods:</i></b> Thirty-five male Wistar rats were randomly divided into 5 groups (<i>n</i> = 7 in each): control, Alzheimer’s disease model that received the beta-amyloid (Aβ) peptide (Alz), Alz + nano-chitosan (NP) Alz + CBD, and Alz + NP + CBD. Alz was induced by injection of the Aβ1-42 peptide into the hippocampal area cornu ammonis1. After confirmation of Alz, 1 μL of CBD and NP + CBD were administered by oral gavage daily in rats for 1 month. The Morris water maze (MWM) test was used to assess learning and memory of animals. Cresyl violet staining was used for consideration of dead cells. Gene and protein expression of CB1 and CB2 was performed by real-time PCR and immunohistochemistry methods. <b><i>Results:</i></b> Induction of Alz significantly increased Aβ plaques and dead cells compared to the control group (<i>p</i> &#x3c; 0.001). Results of MWM in the day test show that Alz + NP + CBD significantly decrease escape latency (<i>p</i> &#x3c; 0.01), travelled distance (<i>p</i> &#x3c; 0.001), and significantly increased spending time (<i>p</i> &#x3c; 0.001) compared to the Alz group. Protein expression of CB1 and CB2 significantly increased in Alz + CBD and Alz + NP + CBD compared to the Alz group (<i>p</i> &#x3c; 0.05). <b><i>Conclusion:</i></b> It seems that CBD coated by nano-chitosan has good potential for reducing Aβ plaques, increasing brain CB1 and levels CB2, and improving learning and memory in Alz rats.


2021 ◽  
pp. 1-14
Author(s):  
Mi Su ◽  
Yongyan Song

<b><i>Background:</i></b> Genetic factors were suggested to have influence on the development of post-traumatic stress disorder (PTSD). The possible association between catechol-O-methyltransferase (<i>COMT</i>) Val158Met polymorphism and PTSD has been evaluated in several studies. But the results were still controversial. Therefore, we conduct this meta-analysis to address these issues. <b><i>Methods:</i></b> The PubMed, EMBASE, Cochrane Library, and Web of Science databases were searched for eligible studies. The pooled odds ratio (OR) with 95% confidence interval (CI) was calculated to estimate the association between <i>COMT</i> Val158Met polymorphism and PTSD. <b><i>Results:</i></b> Five articles including 6 studies with 893 cases and 968 controls were finally included in the present meta-analysis. The pooled analyses did not demonstrate a significant association between the <i>COMT</i> Val158Met polymorphism and PTSD in any of the selected genetic models: allele model (OR = 1.13, 95% CI: 0.97–1.31), dominant model (OR = 1.17, 95% CI: 0.93–1.46), recessive model (OR = 1.44, 95% CI: 0.78–2.66), and additive model (OR = 1.54, 95% CI: 0.85–2.80). Subgroup analyses suggested that the Hardy-Weinberg equilibrium status of genotype distributions could influence the relationship of <i>COMT</i> Val158Met polymorphism and PTSD. <b><i>Conclusions:</i></b> The present meta-analysis suggested that the <i>COMT</i> Val158Met polymorphism may not be associated with the PTSD risk. Further large-scale and population-representative studies are warranted to evaluate the impact of the <i>COMT</i> Val158Met polymorphism on the risk of PTSD.


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