Progress in Neuro-Psychopharmacology & Biological Psychiatry最新文献

{"title":"From brain connectivity to cognitive function: Dissecting the salience network in pediatric BECTS-ESES","authors":"","doi":"10.1016/j.pnpbp.2024.111110","DOIUrl":"10.1016/j.pnpbp.2024.111110","url":null,"abstract":"<div><h3>Background</h3><p>Benign childhood epilepsy with centrotemporal spikes (BECTS), a common pediatric epilepsy, may lead to cognitive decline when compounded by Electrical Status Epilepticus during Sleep (ESES). Emerging evidence suggests that disruptions in the Salience Network (SN) contribute significantly to the cognitive deficits observed in BECTS-ESES. Our study rigorously investigates the dynamic functional connectivity (dFC) within the SN and its correlation with cognitive impairments in BECTS-ESES, employing advanced neuroimaging and neuropsychological assessments.</p></div><div><h3>Methods</h3><p>In this research, 45 patients diagnosed with BECTS-ESES and 55 age-matched healthy controls (HCs) participated. We utilized resting-state functional magnetic resonance imaging (fMRI) and Independent Component Analysis (ICA) to identify three fundamental SN nodes: the right Anterior Insula (rAI), left Anterior Insula (lAI), and the Anterior Cingulate Cortex (ACC). A two-sample <em>t</em>-test facilitated the comparison of dFC between these pivotal regions and other brain areas.</p></div><div><h3>Results</h3><p>Significantly, the BECTS-ESES group demonstrated increased dFC, particularly between the ACC and the right Middle Occipital Gyrus, and from the rAI to the right Superior Parietal Gyrus and Cerebellum, and from the lAI to the left Postcentral Gyrus. Such dFC augmentations provide neural insights potentially explaining the neuropsychological deficits in BECTS-ESES children. Employing comprehensive neuropsychological evaluations, we mapped these dFC disruptions to specific cognitive impairments encompassing memory, executive functioning, language, and attention. Through multiple regression analysis and path analysis, a preliminary but compelling association was discovered linking dFC disturbances directly to cognitive impairments. These findings underscore the critical role of SN disruptions in BECTS-ESES cognitive dysfunctions.</p></div><div><h3>Limitation</h3><p>Our cross-sectional design and analytic methods preclude definitive mediation models and causal inferences, leaving the precise nature of dFC's mediating role and its direct impact by BECTS-ESES partially unresolved. Future longitudinal and confirmatory studies are needed to comprehensively delineate these associations.</p></div><div><h3>Conclusion</h3><p>Our study heralds dFC within the SN as a vital biomarker for cognitive impairment in pediatric epilepsy, advocating for targeted cognitive-specific interventions in managing BECTS-ESES. The preliminary nature of our findings invites further studies to substantiate these associations, offering profound implications for the prognosis and therapeutic strategies in BECTS-ESES, thereby underlining the importance of this research in the field of pediatric neurology and epilepsy management.</p></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141789888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human CYP2D6 varies across the estrous cycle in brains of transgenic mice altering drug response","authors":"","doi":"10.1016/j.pnpbp.2024.111108","DOIUrl":"10.1016/j.pnpbp.2024.111108","url":null,"abstract":"<div><p>Cytochrome P450 (CYP) 2Ds are drug metabolizing enzymes found in brain and liver which metabolize numerous centrally acting drugs. Inhibition and induction of CYP2D-mediated metabolism in rodent brain alters brain drug and metabolite concentrations and resulting drug response. In female rats, brain CYP2D metabolism varies across the estrous cycle and with exogenous estrogen, changing brain drug concentrations and response.</p><p>In this study harmine-induced hypothermia was lower in humanized CYP2D6 transgenic female mice during estrus compared to diestrus. Pretreatment into the cerebral ventricles with propranolol, a selective irreversible inhibitor of human CYP2D6 in brain, increased hypothermia in estrus but not in diestrus. <em>In vivo</em> enzyme activity was higher in brains of transgenic mice in estrus compared to diestrus and was lower after pretreatment with inhibitor in estrus, but not in diestrus. Hepatic activity and plasma harmine concentrations were unaffected by either estrous phase or inhibition of brain CYP2D6. In wild-type female mice, harmine-induced hypothermia was unaffected by either estrous phase or inhibitor pretreatment. Male mice were used as positive controls, where pretreatment with inhibitor increased harmine-induced hypothermia in transgenic but not wild-type, mice.</p><p>This study provides evidence for female hormone cycle-based regulation of drug metabolism by human CYP2D6 in brain and resulting drug response. This suggests that brain CYP2D6 metabolism may vary, for example, during the menstrual cycle, pregnancy, or menopause, or while taking oral contraceptives or hormone therapy. This variation could contribute to individual differences in response to centrally acting CYP2D6-substrate drugs by altering local brain drug and/or metabolite concentrations.</p></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141789889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Delayed effects of alcohol consumption on the association between serum BDNF levels and post-traumatic stress disorder development over two-years","authors":"","doi":"10.1016/j.pnpbp.2024.111106","DOIUrl":"10.1016/j.pnpbp.2024.111106","url":null,"abstract":"<div><h3>Backgrounds</h3><p>This study aimed to examine the individual and combined effects of serum BDNF (sBDNF) levels and alcohol consumption status, assessed shortly after a physical injury, on the development of post-traumatic stress disorder (PTSD) over two years.</p></div><div><h3>Methods</h3><p>Participants were consecutively recruited from a trauma center and followed prospectively for two years. At baseline, sBDNF levels and alcohol consumption history were assessed. A range of socio-demographic and clinical covariates were also collected. PTSD diagnosis during follow-up (3, 6, 12, and 24 months post-injury) was established using the Clinician-Administered PTSD Scale for DSM-5. Binary and multinomial logistic regression analyses were employed to investigate the relationships between sBDNF levels, alcohol consumption status, and PTSD onset.</p></div><div><h3>Results</h3><p>Out of 923 participants analyzed, 112 (12.1%) developed PTSD at some point during the study, with prevalence rates of 8.8% at 3 months, 7.6% at 6 months, 4.8% at 12 months, and 3.7% at 24 months. The study found no individual associations between sBDNF levels or alcohol consumption status and PTSD development. However, lower sBDNF levels significantly predicted PTSD in individuals who consumed alcohol, a relationship not observed in non-drinkers, with significant interaction terms. This pattern was consistent at later follow-up points from 12 to 24 months, but not at earlier assessments at 3 and 6 months.</p></div><div><h3>Limitations</h3><p>The study's reliance on participants from a single trauma center with moderate to severe injuries may limit the generalizability of the findings.</p></div><div><h3>Conclusions</h3><p>A significant interaction between sBDNF levels and alcohol consumption in relation to PTSD development was observed, particularly in the long term. These findings highlight the necessity of considering both sBDNF levels and alcohol consumption in strategies aimed at preventing PTSD among individuals with physical injuries, underscoring the need for tailored approaches based on these factors.</p></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141789887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dihydroartemisinin promotes tau O-GlcNAcylation and improves cognitive function in hTau transgenic mice","authors":"","doi":"10.1016/j.pnpbp.2024.111105","DOIUrl":"10.1016/j.pnpbp.2024.111105","url":null,"abstract":"<div><p>Tauopathy is a collective term for several neurodegenerative diseases characterized by the intracellular accumulation of hyperphosphorylated microtubule-associated protein Tau (P-tau). Our recent report has revealed the neuroprotective effect of dihydroartemisinin (DHA) on mice overexpressing human Tau (hTau) in the hippocampus by enhancing O-linked-N-Acetylglucosaminylation (O-GlcNAcylation) modification. However, whether DHA can improve synaptic and cognitive function in hTau transgenic mice by specifically promoting Tau O-GlcNAcylation is still unclear. Here, we introduced hTau transgenic mice, a more optimal tauopathy model, to study the effect of DHA on Tau O-GlcNAcylation. We reported that DHA treatment alleviated the deficits of hippocampal CA1 LTP and spatial learning and memory in the Barnes maze and context fear conditioning tests in hTau transgenic mice. Mechanically, we revealed that DHA exerted a significant protective effect by upregulating Tau O-GlcNAcylation and attenuating Tau hyperphosphorylation. Through molecular docking, we found a stable binding between DHA and O-GlcNAc transferase (OGT). We further reported that DHA treatment had no effect on the expression of OGT, but it promoted OGT nuclear export, thereby enhancing OGT-mediated Tau O-GlcNAcylation. Taken together, these results indicate that DHA exerts neuroprotective effect by promoting cytoplasmic translocation of OGT and rebuilding the balance of Tau O-GlcNAcylation/phosphorylation, enhancing O-GlcNAcylation of Tau, suggesting that DHA may be a potential therapeutic agent against tauopathy.</p></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141762674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the interplay between addiction and time perception: A systematic review and meta-analysis","authors":"","doi":"10.1016/j.pnpbp.2024.111104","DOIUrl":"10.1016/j.pnpbp.2024.111104","url":null,"abstract":"<div><p>Prior studies have investigated the immediate impacts of substances on temporal perception, the impact of temporal outlook, and the consequences of modified temporal perception on addictive behaviors. These inquiries have provided valuable perspectives on the intricate associations between addiction and time perception, enriching the groundwork for forthcoming research and therapeutic strategies. This comprehensive review aims to further explore intricate correlation among diverse addictive substances—namely alcohol, cannabis, nicotine, opioids—and non-substance addictions such as internet gaming, elucidating their influence on temporal perception. Adhering to the PICOS method and adhering to PRISMA guidelines, we systematically reviewed and critically evaluated all existing research concerning temporal perception in individuals with substance and non-substance use disorders. Specifically, our analyses involved 31 pertinent articles encompassing six unique groups—alcohol, nicotine, cannabis, stimulants, opioids, and internet-related addictions—sourced from a pool of 551 papers. The findings revealed differences in time perception between addicts and control groups, as indicated by medium to large effect sizes (Hedge's g = 0.8, <em>p</em> &lt; 0.001). However, the nature of these differences—whether they predominantly involve time overestimation or underestimation—is not yet definitively clear. This variability underscores the complexity of the relationship between addiction and temporal perception, paving the way for further research to unravel these intricate dynamics.</p></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141762622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex-dependent nonlinear Granger connectivity patterns of brain aging in healthy population","authors":"","doi":"10.1016/j.pnpbp.2024.111088","DOIUrl":"10.1016/j.pnpbp.2024.111088","url":null,"abstract":"<div><h3>Background</h3><p>Brain aging is a complex process that involves functional alterations in multiple subnetworks and brain regions. However, most previous studies investigating aging-related functional connectivity (FC) changes using resting-state functional magnetic resonance images (rs-fMRIs) have primarily focused on the linear correlation between brain subnetworks, ignoring the nonlinear casual properties of fMRI signals.</p></div><div><h3>Methods</h3><p>We introduced the neural Granger causality technique to investigate the sex-dependent nonlinear Granger connectivity (NGC) during aging on a publicly available dataset of 227 healthy participants acquired cross-sectionally in Leipzig, Germany.</p></div><div><h3>Results</h3><p>Our findings indicate that brain aging may cause widespread declines in NGC at both regional and subnetwork scales. These findings exhibit high reproducibility across different network sparsities, demonstrating the efficacy of static and dynamic analysis strategies. Females exhibit greater heterogeneity and reduced stability in NGC compared to males during aging, especially the NGC between the visual network and other subnetworks. Besides, NGC strengths can well reflect the individual cognitive function, which may therefore work as a sensitive metric in cognition-related experiments for individual-scale or group-scale mechanism understanding.</p></div><div><h3>Conclusion</h3><p>These findings indicate that NGC analysis is a potent tool for identifying sex-dependent brain aging patterns. Our results offer valuable perspectives that could substantially enhance the understanding of sex differences in neurological diseases in the future, especially in degenerative disorders.</p></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141735705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cognitive changes in patients with unipolar TRD treated with IV ketamine: A systematic review","authors":"","doi":"10.1016/j.pnpbp.2024.111095","DOIUrl":"10.1016/j.pnpbp.2024.111095","url":null,"abstract":"<div><h3>Background</h3><p>Unipolar treatment-resistant depression (MDD-TRD) is associated with neurocognitive impairment. Ketamine, an emerging treatment for MDD-TRD, may have neurocognitive benefits, but evidence remains limited.</p></div><div><h3>Methods</h3><p>We conducted a systematic search on EMBASE, Google Scholar, PsycINFO, and PubMed and included studies exploring the cognitive effects of intravenous (IV) ketamine treatment in the management of MDD-TRD following the PRISMA guidelines. We analyzed cognitive scale score changes pre- and post-IV ketamine treatment and the quality of the evidence using the Cochrane risk of bias tool and the Grading of Recommendations Assessment, Development, and Evaluation (GRADE).</p></div><div><h3>Results</h3><p>Out of 1171 identified studies, fourteen studies were included in this study. Most studies reported positive cognitive outcomes post-ketamine treatment, including improvements in processing speed, working memory, verbal and visual memory, executive function, attention, emotional processing, and auditory verbal episodic memory. Variability existed, with one study reporting negative effects on verbal memory. Overall, studies exhibited a low risk of bias.</p></div><div><h3>Limitations</h3><p>Several limitations impacted the results observed, including confining our scope to articles in English, heterogeneity of the included studies, small sample sizes, and the predominance of a female, Western, and Caucasian population, constraining the generalizability of the findings.</p></div><div><h3>Conclusions</h3><p>IV ketamine treatment shows promise in improving neurocognitive function in MDD-TRD patients. However, further research is warranted to elucidate long-term effects, control for confounders such as concomitant medications, and explore neurocognitive subgroups within the TRD population. These findings underscore the need for comprehensive assessment and management of cognitive symptoms in TRD, informing future clinical practice.</p></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0278584624001635/pdfft?md5=30734d6207c621eb9fdcd07de322e07e&pid=1-s2.0-S0278584624001635-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141735704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Semaglutide ameliorated autism-like behaviors and DNA repair efficiency in male BTBR mice by recovering DNA repair gene expression","authors":"","doi":"10.1016/j.pnpbp.2024.111091","DOIUrl":"10.1016/j.pnpbp.2024.111091","url":null,"abstract":"<div><p>Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder that is marked by impaired social interactions, and increased repetitive behaviors. There is evidence of genetic changes in ASD, and several of these altered genes are linked to the process of DNA repair. Therefore, individuals with ASD must have improved DNA repair efficiency to mitigate risks associated with ASD. Despite numerous milestones in ASD research, the disease remains incurable, with a high occurrence rate and substantial financial burdens. This motivates scientists to search for new drugs to manage the disease. Disruption of glucagon-like peptide-1 (GLP-1) signaling, a regulator in neuronal development and maintains homeostasis, has been associated with the pathogenesis and progression of several neurological disorders, such as ASD. Our study aimed to assess the impact of semaglutide, a new GLP-1 analog antidiabetic medication, on behavioral phenotypes and DNA repair efficiency in the BTBR autistic mouse model. Furthermore, we elucidated the underlying mechanism(s) responsible for the ameliorative effects of semaglutide against behavioral problems and DNA repair deficiency in BTBR mice. The current results demonstrate that repeated treatment with semaglutide efficiently decreased autism-like behaviors in BTBR mice without affecting motor performance. Semaglutide also mitigated spontaneous DNA damage and enhanced DNA repair efficiency in the BTBR mice as determined by comet assay. Moreover, administering semaglutide recovered oxidant-antioxidant balance in BTBR mice. Semaglutide restored the disrupted DNA damage/repair pathways in the BTBR mice by reducing Gadd45a expression and increasing Ogg1 and Xrcc1 expression at both the mRNA and protein levels. This suggests that semaglutide holds great potential as a novel therapeutic candidate for treating ASD traits.</p></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141732377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disruption of relapse to cocaine and morphine seeking by LiCl-induced aversive counterconditioning following memory retrieval","authors":"","doi":"10.1016/j.pnpbp.2024.111094","DOIUrl":"10.1016/j.pnpbp.2024.111094","url":null,"abstract":"<div><p>Substance use disorder is conceptualized as a form of maladaptive learning, whereby drug-associated memories, elicited by the presence of stimuli related to drug contexts or cues, contribute to the persistent recurrence of craving and the reinstatement of drug-seeking behavior. Hence, use of pharmacology or non-pharmacology way to disrupt drug-related memory holds promise to prevent relapse. Several studies have shown that memories can be unstable and susceptible to modification during the retrieval reactivation phase, termed the “reconsolidation time window”. In this study, we use the classical conditioned place preference (CPP) model to investigate the role of aversive counterconditioning on drug-related memories during reconsolidation. Specifically, we uncovered that reconditioning drug cues through counterconditioning with LiCl-induced aversive outcomes following drug memory retrieval reduces subsequent drug-seeking behavior. Notably, the recall of cocaine- or morphine-CPP was eliminated when LiCl-induced aversive counterconditioning was performed 10 min, but not 6 h (outside the reconsolidation time window) after cocaine or morphine memory retrieval. In addition, the effect of LiCl-induced aversive counterconditioning could last for about 14 days. These results suggest that aversive counterconditioning during the reconsolidation of cocaine or morphine memory can prevent the re-seeking of cocaine or morphine, presumably by updating or replacing cocaine or morphine memories with aversive information.</p></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141639728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The influence of novelty detection on the 40-Hz auditory steady-state response in schizophrenia: A novel hypothesis from meta-analysis","authors":"","doi":"10.1016/j.pnpbp.2024.111096","DOIUrl":"10.1016/j.pnpbp.2024.111096","url":null,"abstract":"<div><p>The 40-Hz auditory steady-state response (ASSR) is influenced not only by parameters such as attention, stimulus type, and analysis level but also by stimulus duration and inter-stimulus interval (ISI). In this meta-analysis, we examined these parameters in 33 studies that investigated 40-Hz ASSRs in patients with schizophrenia. The average Hedges' g random effect sizes were − 0.47 and − 0.43 for spectral power and phase-locking, respectively. We also found differences in ASSR measures based on stimulus duration and ISI. In particular, ISI was shown to significantly influence differences in the 40-Hz ASSR between healthy controls and patients with schizophrenia. We proposed a novel hypothesis focusing on the role of novelty detection, dependent on stimulus duration and ISI, as a critical factor in determining these differences. Specifically, longer stimulus durations and shorter ISIs under random presentation, or shorter stimulus durations and longer ISIs under repetitive presentation, decrease the 40-Hz ASSR in healthy controls. Patients with schizophrenia show minimal changes in response to stimulus duration and ISI, thus reducing the difference between controls and patients. This hypothesis can consistently explain most of the studies that have failed to show a reduction in 40-Hz ASSR in patients with schizophrenia. Increased novelty-related activity, reflected as an increase in auditory evoked potential components at stimulus onset, such as the N1, could suppress the 40-Hz ASSR, potentially reducing the peak measures of spectral power and phase-locking. To establish the 40-Hz ASSR as a truly valuable biomarker for schizophrenia, further systematic research using paradigms with various stimulus durations and ISIs is needed.</p></div>","PeriodicalId":54549,"journal":{"name":"Progress in Neuro-Psychopharmacology & Biological Psychiatry","volume":null,"pages":null},"PeriodicalIF":5.3,"publicationDate":"2024-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0278584624001647/pdfft?md5=353d9f22f9ddcb3e611587dcfcf5fda0&pid=1-s2.0-S0278584624001647-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141639901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}