International Journal of Neuropsychopharmacology最新文献

{"title":"In memoriam: Professor Shigeto Yamawaki (January 15, 1954-June 8, 2026)-a visionary leader connecting Japan, Asia, and the world.","authors":"Kazutaka Ikeda, Gabriella Gobbi, Joseph Zohar, Gregers Wegener, Pierre Blier, Siegfried Kasper, John H Krystal, Anthony Phillips, Hans-Jürgen Möller, Toshikazu Saito, Hiroyuki Uchida, Atsumi Nitta, Go Okada","doi":"10.1093/ijnp/pyag038","DOIUrl":"https://doi.org/10.1093/ijnp/pyag038","url":null,"abstract":"","PeriodicalId":14134,"journal":{"name":"International Journal of Neuropsychopharmacology","volume":"29 8","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148792724","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":"Global perspectives on central nervous system drug innovation: achievements, barriers, and priorities for the next decade.","authors":"Hiroyuki Uchida, Gabriella Gobbi, Joseph Zohar, Allan H Young, Dan Rujescu, Ming-Chyi Huang, Suresh Sundram, Lukoye Atwoli, Jana Vukovic, Kazutaka Ikeda","doi":"10.1093/ijnp/pyag023","DOIUrl":"10.1093/ijnp/pyag023","url":null,"abstract":"<p><strong>Background: </strong>Over the past decade, neuropsychopharmacology has shifted from stagnation to momentum, with first-in-class mechanisms and biomarker-enabled trials spanning psychiatry and neurology.</p><p><strong>Methods: </strong>We narratively synthesized advances from 2013 to 2026 across central nervous system (CNS) discovery and development, including pivotal trials, regulatory actions, digital/real-world evidence, genetics, artificial intelligence (AI), and implementation/global-access themes that are endorsed by international societies.</p><p><strong>Results: </strong>Therapeutic gains include rapid-acting drugs for treatment-resistant depression (intranasal esketamine); psychedelic-assisted therapy for posttraumatic stress disorder and depression; neuroactive steroid γ-aminobutyric acid-A receptor positive allosteric modulators (brexanolone, zuranolone) for postpartum depression; non-dopaminergic muscarinic agonists (xanomeline-trospium) for schizophrenia; orexin receptor antagonists for insomnia; and anti-amyloid monoclonal antibodies (lecanemab, donanemab) for early Alzheimer's disease. Persistent barriers include high mid-/late-stage attrition that is driven by placebo effects, subjective endpoints, and preclinical-to-clinical gaps; regulatory and economic headwinds; and limited generalizability from tightly run trials. Emerging enablers include adaptive/platform designs, digital health technologies, patient-reported outcomes, and clinical outcome assessments, real-world evidence (RWE), AI/machine learning (ML), genetics for target de-risking and biomarker-guided stratification, and publicly accessible large CNS relevant biological datasets.</p><p><strong>Conclusions: </strong>To convert momentum into durable progress, we recommend: (1) deeper academia-industry/stakeholder collaboration and sustained funding for high-risk/high-reward science from industry, governments, and non-for profit foundations; (2) modernized regulation (flexible evidentiary paths, novel endpoints, and clear guidance on adaptive/platform trials); (3) data-driven development integrating RWE, AI/ML, and precision medicine; (4) the adoption of Neuroscience-based Nomenclature; and (5) a global-access mandate with essential-medicine inclusion, equitable pricing/licensing, capacity building, tele-enabled mental health, and geographically diverse research. Aligning scientific innovation with implementation and equity can accelerate translation and ensure new treatments benefit patients worldwide.</p>","PeriodicalId":14134,"journal":{"name":"International Journal of Neuropsychopharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13499527/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147837682","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":"External validation as the critical step for predictive biomarkers.","authors":"Pál Czobor, Brigitta Kakuszi, Máté Fullajtár, István Bitter","doi":"10.1093/ijnp/pyag036","DOIUrl":"10.1093/ijnp/pyag036","url":null,"abstract":"","PeriodicalId":14134,"journal":{"name":"International Journal of Neuropsychopharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13358870/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148329081","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":"Correction to: Stress-induced altered expression of hippocampal nuclear and mitochondrial encoded genes in rats and cross-species genetic associations reveal molecular links to depression.","authors":"","doi":"10.1093/ijnp/pyag039","DOIUrl":"10.1093/ijnp/pyag039","url":null,"abstract":"","PeriodicalId":14134,"journal":{"name":"International Journal of Neuropsychopharmacology","volume":"29 7","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13393888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148578574","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":"Recent cannabis exposure and acute nicotine effects: insights from randomized, double-blind, placebo-controlled intravenous nicotine studies.","authors":"Gabriel P A Costa, R Ross MacLean, Mehmet Sofuoglu, Joao P De Aquino","doi":"10.1093/ijnp/pyag030","DOIUrl":"10.1093/ijnp/pyag030","url":null,"abstract":"<p><strong>Objective: </strong>Cannabis-nicotine co-use is common and may affect cessation outcomes, yet whether recent cannabis exposure alters nicotine's acute effects in humans remains unclear. We examined whether recent, non-daily cannabis exposure modulates the acute subjective effects of intravenous (IV) nicotine.</p><p><strong>Methods: </strong>We pooled data from 2 randomized, double-blind, placebo-controlled studies using IV nicotine to isolate nicotine's pharmacodynamics in adults who smoke tobacco cigarettes (N = 60). Participants completed 3 sessions (placebo, 0.1 mg, 0.2 mg nicotine/70 kg). Recent cannabis exposure was defined a priori (past-30-day use with positive urine 11-nor-9-carboxy-delta-9-tetrahydrocannabinol vs no past-30-day use with negative screen). Primary outcomes were peak Drug Effects Questionnaire (DEQ) composites-stimulatory, pleasurable, aversive-within 10 minutes post-infusion. Secondary outcomes included nicotine self-administration behavior (proportion of nicotine choices) and cardiovascular responses (heart rate, blood pressure). Linear mixed-effects models included dose, cannabis exposure, sex, and FTND.</p><p><strong>Results: </strong>Nicotine increased all DEQ domains dose-dependently (P < .0001). Aversive effects showed a significant dose x cannabis exposure interaction (χ2 = 13.31, P = .001): participants with recent cannabis exposure reported greater aversive responses at 0.2 mg (Cohen's d' = 0.83), with minimal between-group differences at placebo/0.1 mg. Nicotine self-administration did not differ by cannabis exposure status, and no dose x cannabis exposure interactions were observed for cardiovascular responses.</p><p><strong>Conclusions: </strong>Recent, non-daily cannabis exposure is thus associated with selectively greater aversive responses to a clinically relevant IV nicotine dose, without differential cardiovascular reactivity or altered nicotine choice. These findings support a shift in the aversive limb of nicotine's dose-response and inform mechanistic and clinical studies on how cannabis exposure shapes nicotine reinforcement and cessation outcomes.</p><p><strong>Clinical trial registration: </strong>NCT01495819, https://clinicaltrials.gov/study/NCT01495819.</p>","PeriodicalId":14134,"journal":{"name":"International Journal of Neuropsychopharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13322297/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148030028","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":"Genetic overlap between treatment-resistant schizophrenia and smoking initiation.","authors":"Elise Koch, Nadine Parker, Helin H Mohammad, Hasan Ç Lenk, Lars A R Ystaas, Piotr Jaholkowski, Alexey A Shadrin, Oleksandr Frei, Anders M Dale, Srdjan Djurovic, Espen Molden, Kevin S O'Connell, Ole A Andreassen","doi":"10.1093/ijnp/pyag035","DOIUrl":"10.1093/ijnp/pyag035","url":null,"abstract":"<p><strong>Background: </strong>Early detection of treatment-resistant schizophrenia (TRS) is of substantial clinical importance. While TRS is heritable, the associated genetic variants have been difficult to identify. Cigarette smoking is associated with non-response to antipsychotics, and smoking behavior and schizophrenia have a shared genetic basis. Thus, TRS may also have a shared genetic basis with smoking behavior.</p><p><strong>Objective: </strong>Here, we aim to identify genetic variants associated with TRS by leveraging overlapping genetic variants with smoking initiation to increase statistical power.</p><p><strong>Methods: </strong>We analyzed genome-wide data for TRS and smoking initiation with the conditional/conjunctional false discovery rate (cond/conjFDR) to identify shared loci, and LD score regression to determine genetic correlations. To investigate potential causal effects of shared loci, we performed Mendelian randomization analyses. Shared loci were mapped to genes, which were further investigated for enrichment of drug target genes.</p><p><strong>Results: </strong>We observed a significant positive genetic correlation between TRS and smoking initiation (rg = 0.47 P = .0002). Leveraging the genetic overlap between TRS and smoking initiation, we identified four novel loci jointly associated with TRS and smoking initiation. The condFDR results improved polygenic prediction of TRS. Mendelian randomization indicates putative evidence for a causal effect of genetic liability to TRS on smoking initiation. The functional genetic analyses suggest that alpha-1-adrenergic receptors may be involved in the pathophysiology of TRS and possibly related to the efficacy of clozapine versus other antipsychotic drugs.</p><p><strong>Conclusion: </strong>In conclusion, our results show that shared genetic mechanisms influence both TRS and smoking behavior, which provide new insights into the biological underpinnings of TRS.</p>","PeriodicalId":14134,"journal":{"name":"International Journal of Neuropsychopharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13358876/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148345336","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":"Ketamine effects on EEG and their links to therapy differ across treatment-resistant major depression, post-traumatic stress disorder, and obsessive-compulsive disorder.","authors":"Shabah M Shadli, Neda Nasrollahi, Calvin K Young, Gabrielle S R Schuck, Meadow G Whatson, Tame N J Kawe, Shona Neehoff, Ben Beaglehole, Paul Glue, Neil McNaughton","doi":"10.1093/ijnp/pyag037","DOIUrl":"10.1093/ijnp/pyag037","url":null,"abstract":"<p><strong>Introduction: </strong>Neurotic disorders-major depressive disorder (MDD), panic disorder, social anxiety disorder, generalized anxiety disorder, obsessive-compulsive disorder (OCD), post-traumatic stress disorder (PTSD), and specific phobia-have differing pharmaceutical profiles. But all, even when resistant to conventional treatment (TR), respond quickly to low-dose (0.5-1.0 mg/kg I.M.) ketamine. We explore the variation in the neural effects of ketamine across its treatments of TR-MDD, TR-PTSD, and TR-OCD.</p><p><strong>Materials and methods: </strong>We recorded 10 min of resting frontal activity and diagnosis-related scale measures, before and 2 h after fentanyl (50 mcg) or ketamine (0.5 or 1.0 mg/kg, I.M.) counterbalanced across 3 sessions at least a week apart. Average power spectra were calculated for delta, theta, alpha1, alpha2, beta, and gamma bands. Analysis of variance compared TR-PTSD (20 F, 2 M) with TR-MDD (12 F, 13 M). Preliminary TR-OCD (5 F, 2 M) data were also obtained.</p><p><strong>Results: </strong>TR-PTSD patients showed dose- and band frequency-dependent electroencephalography (EEG) power changes (particularly alpha at 0.05 mg/kg), while TR-MDD patients did not. TR-OCD differed qualitatively from both. The correlation of power change with score change was maximal for different bands and electrodes across the different scales (Impact of Events Scale-Revised, Montgomery-Åsberg Depression Rating Scale, Hospital Anxiety and Depression Scales, Hamilton Anxiety Scale, Fear Questionnaire, and Yale-Brown Obsessive-Compulsive Scale).</p><p><strong>Discussion: </strong>Ketamine effects and their therapeutic links vary in band and site with conventional diagnosis-including previous TR anxiety results. The EEG results appear to detect changes in the disorder-specific systems that conventional treatments target selectively and directly and these appear to require a ketamine-sensitive factor (as a \"double hit\") to generate disorder.</p>","PeriodicalId":14134,"journal":{"name":"International Journal of Neuropsychopharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13425232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390726","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":"Secondary Restless Legs Syndrome during psychopharmacological treatment: real-world evidence from a multinational pharmacovigilance program.","authors":"Gernot Fugger, Ulrich Rabl, Lucie Bartova, Valentin Popper, Victoria Watzal, Dominik Ivkic, Jakob Donath, Constance Busvine, Waldemar Greil, Sermin Toto, Renate Grohmann, Richard Frey, Anastasios Konstantinidis, Andreas Erfurth, Siegfried Kasper","doi":"10.1093/ijnp/pyag029","DOIUrl":"10.1093/ijnp/pyag029","url":null,"abstract":"<p><strong>Objective: </strong>Secondary Restless Legs Syndrome (RLS) has repeatedly been associated with psychopharmacotherapy, especially antidepressants and antipsychotics. However, existing evidence is conflicting in terms of the magnitude of the association as well as the significance of substance classes or individual compounds. The objective of the present study was to evaluate secondary RLS linked to psychotropic medication in real-world, inpatient clinical routine treatment settings.</p><p><strong>Methods: </strong>A large dataset from a multinational pharmacovigilance program in German-speaking countries (Arzneimittelsicherheit in der Psychiatrie, \"Drug safety in Psychiatry\") from January 2001 to December 2016 was retrospectively analyzed.</p><p><strong>Results: </strong>In a total of 340 099 monitored inpatients, 67 cases of newly diagnosed and severe RLS related to psychotropic drug treatment were recorded equivalent to a relative frequency of 0.02%. Over 80% of the cases were attributable to two compounds: the antidepressant mirtazapine and the antipsychotic quetiapine. Mirtazapine was found in 39 patients, while quetiapine was found in 16 patients with secondary RLS. For both substances, drug dosages were generally low at onset of secondary RLS. Most cases exhibited an onset within 1 or 2 days after dosage start or change.</p><p><strong>Conclusion: </strong>Histamine neurotransmission may represent a crucial common denominator in terms of secondary RLS in association with psychopharmacotherapeutics, as both substances exhibit antihistamingeric effects at lower dosages.</p>","PeriodicalId":14134,"journal":{"name":"International Journal of Neuropsychopharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13326631/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148198785","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":"PDE4A knockdown rescues alcohol-induced cognitive impairment and synaptic dysfunction via the cAMP/PKA/CREB pathway.","authors":"Huan Tu, Rongzhen Sun, Shengyao Ma, Chunxu Li, Mingti Lv, Mei Han, Han-Ting Zhang","doi":"10.1093/ijnp/pyag031","DOIUrl":"10.1093/ijnp/pyag031","url":null,"abstract":"<p><strong>Background: </strong>Alcoholic dementia (AlD) is a severe neurological disorder with no effective treatment. Development of pan-phosphodiesterase-4 (PDE4) inhibitors for clinical treatment of neurological conditions has been hampered by emetic side effects primarily mediated by PDE4D, one of the four subtypes of PDE4. Although PDE4A was shown to be upregulated by chronic alcohol exposure, its therapeutic relevance to AlD remains unclear.</p><p><strong>Methods: </strong>A stable mouse model of AlD was established in 3-month-old 3xTg-AD mice using a free-choice two-bottle protocol (25% alcohol) for 19 weeks. Mice received either rolipram injections for 3 weeks or PDE4A knockdown for 6 weeks. Cognitive function was assessed using the Morris water maze, novel object recognition, and Y-maze tests. Hippocampal neuropathology-including Aβ deposition, synaptic integrity, Tau phosphorylation (at Ser214/Ser404), and neuronal apoptosis-was evaluated by immunofluorescence or immunohistochemistry. Changes in key proteins of the cAMP/PKA/CREB signaling pathway were analyzed by Western blotting.</p><p><strong>Results: </strong>This study demonstrated that selectively targeting PDE4A rescued cognitive and neuropathological deficits in a validated mouse model of AlD. Behavioral tests showed that PDE4A knockdown significantly improved spatial memory and cognition in the Morris water maze, novel object recognition, and the Y maze in the AlD mice. Pathological analysis revealed that PDE4A knockdown reduced amyloid-beta (Aβ) deposition and phosphorylated Tau levels. Furthermore, it restored synaptic integrity, as evidenced by the upregulation of PSD95 and Synaptophysin, enhanced dendritic complexity, and increased spine density, while also exerting neuroprotective effects by suppressing neuronal apoptosis in AlD mice. Mechanistically, the therapeutic benefits of PDE4A knockdown were mediated through the reactivation of the critically impaired cAMP/PKA/CREB signaling pathway, leading to elevated cAMP levels, increased PKA activity, and enhanced phosphorylation of CREB.</p><p><strong>Conclusion: </strong>Our findings established PDE4A as one of the key AlD pathological drivers and identified its selective inhibition as a novel and promising therapeutic strategy for AlD, offering a viable approach to circumvent the adverse effects associated with broad-spectrum PDE4 inhibition.</p>","PeriodicalId":14134,"journal":{"name":"International Journal of Neuropsychopharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13371961/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148421010","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":"Divergent effects of interleukin-6 and ghrelin on remission and relapse in depression treatment.","authors":"Jae-Min Kim, Hee-Ju Kang, Ju-Wan Kim, Min Jhon, Ju-Yeon Lee, Sung-Wan Kim, Il-Seon Shin","doi":"10.1093/ijnp/pyag032","DOIUrl":"https://doi.org/10.1093/ijnp/pyag032","url":null,"abstract":"<p><strong>Background: </strong>This study was to explore how serum ghrelin levels modulate the relationship between interleukin-6 (IL-6) and outcomes of antidepressant treatment, specifically focusing on 12-week remission and 24-month relapse in patients with depressive disorders.</p><p><strong>Methods: </strong>This investigation involved the analysis of baseline serum levels of ghrelin and IL-6 among 1086 patients enrolled in a naturalistic study of stepwise antidepressant therapy. Remission was determined by a Hamilton Depression Rating Scale (HAMD) score of 7 or less at 12 weeks. Those who responded (HAMD score ≤ 14) at this juncture were subsequently monitored for relapse (HAMD score > 14) quarterly over a 24-month period. The study employed logistic regression models, adjusted for various sociodemographic and clinical factors, to evaluate the interaction between these biomarkers and treatment outcomes.</p><p><strong>Results: </strong>Findings revealed that while serum ghrelin levels did not independently affect treatment outcomes, they significantly influenced the association between elevated IL-6 levels and the risks of non-remission at 12 weeks and relapse at 24 months. Specifically, high IL-6 levels correlated with poorer outcomes predominantly in the presence of lower ghrelin levels, with these interactions reaching statistical significance in relapse outcomes post-adjustment.</p><p><strong>Conclusion: </strong>The study highlights the complex interplay between IL-6 and ghrelin in shaping the efficacy of antidepressant treatments, demonstrating divergent influences on remission and relapse. These results emphasize the importance of incorporating multiple biomarkers into predictive models to tailor antidepressant strategies more effectively. Continued research is needed to dissect the underlying dynamics of these biomarker interactions.</p>","PeriodicalId":14134,"journal":{"name":"International Journal of Neuropsychopharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295012","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}