Medical hypotheses最新文献_第7页

HIV-induced neuroinflammation may influence an increase in sexual behavior: A testable hypothesis hiv诱导的神经炎症可能影响性行为的增加：一个可验证的假设

IF 0.8 4区医学

Medical hypotheses Pub Date : 2026-01-01 Epub Date: 2025-12-11 DOI: 10.1016/j.mehy.2025.111850

Aria Ma, Liana Feller, Erik Salgado, Philip T. Starks

引用次数: 0

Brainstem dysfunction as a potential etiology of ME/CFS and long COVID: A mechanical basis 脑干功能障碍作为ME/CFS和长COVID的潜在病因：机械基础

IF 0.8 4区医学

Medical hypotheses Pub Date : 2026-01-01 Epub Date: 2025-11-15 DOI: 10.1016/j.mehy.2025.111812

Jeffrey D. Wood , Thomas F. Varley , Jacob Hartman , Nick Melia , David L. Kaufman , Tess Falor

{"title":"Brainstem dysfunction as a potential etiology of ME/CFS and long COVID: A mechanical basis","authors":"Jeffrey D. Wood , Thomas F. Varley , Jacob Hartman , Nick Melia , David L. Kaufman , Tess Falor","doi":"10.1016/j.mehy.2025.111812","DOIUrl":"10.1016/j.mehy.2025.111812","url":null,"abstract":"<div><div>The underlying mechanism of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) remains poorly understood. Given the dramatic increase in cases following the COVID-19 pandemic, it is important to establish a deeper understanding of the disease. We propose a model of how ME/CFS, and post-infectious syndromes such as long Covid (LC), might emerge following a viral insult. Central to this hypothesis is the recognition that the core diagnostic features of ME/CFS involve physiological systems known to be governed by the brainstem. With emerging literature suggesting that spinal and craniocervical pathologies may be over-represented in people with ME/CFS, we hypothesize that a non-trivial number of cases of ME/CFS and LC may have a “mechanical basis”: In vulnerable individuals, an infection may damage the connective tissue structures responsible for maintaining the physical integrity of the brainstem. This can lead to neuromechanical pathologies such as craniocervical instability (CCI) and intracranial pressure dysregulation that cause mechanical deformation or displacement of the brainstem. The resulting brainstem deformative stress causes autonomic nervous system, immune system, and metabolic dysfunction due to aberrant signaling from deformed brainstem nuclei, leading to the chronic and often lifelong presentation typical of ME/CFS.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"206 ","pages":"Article 111812"},"PeriodicalIF":0.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145622251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bayesian hypothesis generation: a probabilistic framework for evaluating novel hypotheses before data collection 贝叶斯假设生成：在数据收集之前评估新假设的概率框架

IF 0.8 4区医学

Medical hypotheses Pub Date : 2026-01-01 Epub Date: 2025-11-25 DOI: 10.1016/j.mehy.2025.111841

Tan Aik Kah

{"title":"Bayesian hypothesis generation: a probabilistic framework for evaluating novel hypotheses before data collection","authors":"Tan Aik Kah","doi":"10.1016/j.mehy.2025.111841","DOIUrl":"10.1016/j.mehy.2025.111841","url":null,"abstract":"<div><div>Scientific progress depends not only on data but also on the ability to generate and evaluate hypotheses under uncertainty. Conventional frameworks—dominated by binary judgments of “proven” versus “implausible”—struggle in early, high-stakes contexts where evidence is sparse. This paper introduces Bayesian hypothesis generation (BHG), a formal probabilistic framework for structured belief-updating. By defining priors, estimating likelihood ratios, and updating posteriors, BHG replaces intuition-driven reasoning with a transparent method that allows probabilities to evolve dynamically as evidence accrues. Retrospective case studies illustrate its utility. In the early phases of the Nipah virus outbreak, suspicions about <em>Helicobacter pylori</em> and gastric cancer, and the bovine spongiform encephalopathy crisis, BHG could have quantified plausibility before definitive proof, providing a principled basis for precautionary action. A prospective example in retinal micro(nano)plastics—now empirically confirmed in human retina— shows how BHG can separate signal from artifact: a model-derived posterior probability of 2.3 %, though modest, was sufficient to justify further investigation. BHG thus offers a systematic approach to hypothesis management, balancing skepticism with openness. It accelerates the pre-validation phase by highlighting which ideas merit attention, resources, or dismissal. To operationalize BHG, I propose integrating it into journal review policies, funding criteria, computational tools, and training curricula. BHG does not replace empirical validation but complements it, providing a disciplined framework for managing uncertainty. By legitimizing structured probability updating, it enhances science’s ability to recognize emerging risks and explore novel ideas with rigor and efficiency.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"206 ","pages":"Article 111841"},"PeriodicalIF":0.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145622252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Reducing hyper mirroring in misophonia: A proposal for cortico-cortical paired associative stimulation (ccPAS) as a potential intervention for treatment 减少恐音症的过度镜像：皮质-皮质配对联想刺激（ccPAS）作为治疗的潜在干预措施的建议

IF 0.8 4区医学

Medical hypotheses Pub Date : 2026-01-01 Epub Date: 2025-11-24 DOI: 10.1016/j.mehy.2025.111840

Pradeep Dheerendra , Sukhbinder Kumar , Phillip E. Gander , Joel I. Berger , Lars F. Muckli

{"title":"Reducing hyper mirroring in misophonia: A proposal for cortico-cortical paired associative stimulation (ccPAS) as a potential intervention for treatment","authors":"Pradeep Dheerendra , Sukhbinder Kumar , Phillip E. Gander , Joel I. Berger , Lars F. Muckli","doi":"10.1016/j.mehy.2025.111840","DOIUrl":"10.1016/j.mehy.2025.111840","url":null,"abstract":"<div><div>Misophonia, a condition characterized by intense emotional and physiological reactions to specific human-generated sounds, was recently proposed as a disorder of hyper mirroring, in which there is an over-representation of the actions of others. A recent study used rTMS to indirectly reduce the hyperactivity in the anterior insula of people with misophonia, leading to a modest reduction in misophonic distress. But further research is needed to optimize TMS for greater efficacy. Recent TMS studies using a paired associative approach have shown that it could be used to reduce automatic mirroring in healthy controls. We propose the use of ccPAS for reducing the aberrant “hyper” connectivity of the motor cortex, suggested to be associated with mirroring, found in misophonia which is directly accessible to TMS. We hope this theoretically driven neuromodulation approach can take advantage of recent advances in brain stimulation and address the need for developing an effective evidence-based treatment for misophonia.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"206 ","pages":"Article 111840"},"PeriodicalIF":0.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145622250","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Complement overactivation: A potential mechanistic bridge between immunothrombosis and thromboinflammation in venous thromboembolism 补体过度激活：静脉血栓栓塞中免疫血栓形成和血栓炎症之间的潜在机制桥梁

IF 0.8 4区医学

Medical hypotheses Pub Date : 2026-01-01 Epub Date: 2025-12-04 DOI: 10.1016/j.mehy.2025.111846

Pawel Rostoff , Anna Patrycja Majda , Olga Kruszelnicka

{"title":"Complement overactivation: A potential mechanistic bridge between immunothrombosis and thromboinflammation in venous thromboembolism","authors":"Pawel Rostoff , Anna Patrycja Majda , Olga Kruszelnicka","doi":"10.1016/j.mehy.2025.111846","DOIUrl":"10.1016/j.mehy.2025.111846","url":null,"abstract":"<div><div>Venous thromboembolism (VTE), encompassing deep vein thrombosis and pulmonary embolism (PE), remains a major cause of morbidity and mortality despite adequate anticoagulation, implying residual risk driven by mechanisms beyond coagulation. Increasing evidence indicates that the complement system – an ancient arm of innate immunity – intersects with coagulation and inflammation, fueling thromboinflammatory reactions within the venous circulation. Experimental and translational studies demonstrate that complement components, including C3, C5a, and the terminal complement complex (sC5b–9), are not only elevated during acute VTE but also correlate with PE severity, right ventricular dysfunction, and prothrombotic plasma profiles. Additionally, bidirectional interactions between complement and coagulation – particularly the ability of activated factor XI (FXIa) to cleave complement factor H (CFH), thereby amplifying alternative pathway activation – suggest that complement overactivation may serve as a mechanistic bridge linking immunothrombosis and thromboinflammation. Excessive complement activation may act as both an initiator and amplifier of VTE by lowering the activation threshold for clot formation and sustaining inflammatory propagation within the venous environment. The novelty of this hypothesis lies in integrating complement-coagulation crosstalk, NET-mediated feedback loops, and human thrombus composition analyses into a unified model of complement-driven venous thrombogenesis. Targeted complement modulation alone or in synergy with FXI inhibition may represent an innovative therapeutic strategy beyond traditional anticoagulation. Future studies combining advanced imaging, thrombus phenotyping, biomarker-guided risk assessment, and interventional trials are needed to determine whether complement inhibition can attenuate thromboinflammatory activity, reduce thrombus burden, or improve clinical outcomes in VTE.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"206 ","pages":"Article 111846"},"PeriodicalIF":0.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145682314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Beyond metabolic endotoxemia paradigm: The circulating lipopolysaccharidome as a determinant of low-grade inflammation and immunomodulation 超越代谢内毒素血症范式：循环脂多糖组作为低度炎症和免疫调节的决定因素

IF 0.8 4区医学

Medical hypotheses Pub Date : 2026-01-01 Epub Date: 2025-12-07 DOI: 10.1016/j.mehy.2025.111847

Alejandra Vargas-Caraveo, Alejandro Martínez-Martínez

{"title":"Beyond metabolic endotoxemia paradigm: The circulating lipopolysaccharidome as a determinant of low-grade inflammation and immunomodulation","authors":"Alejandra Vargas-Caraveo, Alejandro Martínez-Martínez","doi":"10.1016/j.mehy.2025.111847","DOIUrl":"10.1016/j.mehy.2025.111847","url":null,"abstract":"<div><div>Metabolic endotoxemia refers to the translocation of lipopolysaccharides (LPS) from gut-resident Gram-negative bacteria into the bloodstream, a process associated with low-grade chronic inflammation in several pathologies. Although elevated LPS and pro-inflammatory cytokine levels have been documented in affected patients, LPS is also detectable in healthy individuals without eliciting inflammatory responses.</div><div>Most studies assume that any circulating LPS invariably activates TLR4 and triggers inflammation, overlooking the structural variability of LPS across bacterial species, which may function as either agonists or antagonists. Moreover, repeated exposure to agonistic LPS can induce endotoxin tolerance (ET), a regulatory phenomenon that suppresses subsequent inflammatory signaling.</div><div>Thus, it is necessary to move beyond the simplistic view that modest elevations in LPS invariably drive inflammation and instead examine the structural diversity of LPS translocated into the bloodstream and their ability to modulate immune responses. This requires the isolation, purification, and comprehensive chemical and immunological characterization of circulating LPS. Therefore, the authors propose the term “circulating lipopolysaccharidome (cLPSome)” to describe the heterogeneous pool of LPS molecules present in the bloodstream and their distinct immunomodulatory roles. Recognizing this diversity offers a conceptual framework to better understand how LPS-TLR4 interactions shape host immunity, providing new insight into the mechanisms linking low-grade chronic inflammation with a broad spectrum of associated diseases.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"206 ","pages":"Article 111847"},"PeriodicalIF":0.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145733766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Is CXCL13 a key player of antibody-mediated rejection in kidney transplantation? A hypothesis based on its role in modulating the humoral response CXCL13是否在肾移植中抗体介导的排斥反应中起关键作用？一种基于它在调节体液反应中的作用的假说

IF 0.8 4区医学

Medical hypotheses Pub Date : 2026-01-01 Epub Date: 2025-11-28 DOI: 10.1016/j.mehy.2025.111842

Miguel A. Vázquez-Toledo , Carlos A. Guzmán-Martín , Yaneli Juarez-Vicuña , Iván Zepeda-Quiroz , César Flores-Gama , Fausto Sánchez-Muñoz

{"title":"Is CXCL13 a key player of antibody-mediated rejection in kidney transplantation? A hypothesis based on its role in modulating the humoral response","authors":"Miguel A. Vázquez-Toledo , Carlos A. Guzmán-Martín , Yaneli Juarez-Vicuña , Iván Zepeda-Quiroz , César Flores-Gama , Fausto Sánchez-Muñoz","doi":"10.1016/j.mehy.2025.111842","DOIUrl":"10.1016/j.mehy.2025.111842","url":null,"abstract":"<div><div>Antibody-mediated acute rejection (ABMR) is an immunological response generated by the recipient’s immune system against donor antigens. It is characterized by a robust humoral response, resulting in the formation of high-affinity antibodies and endothelial damage. An important factor in acute rejection is the formation of Tertiary Lymphoid Structures (TLS) that facilitate the interaction between Tfh cells and B cells, leading to the production of high-affinity antibodies.</div><div>CXCL13 is a chemokine known for its ability to recruit B cells. It plays an important role in the formation of these ectopic lymphoid niches, which have been associated with poor prognoses for renal allograft survival. CXCL13 organizes CXCR5<sup>+</sup> lymphocytes and sustains an inflammatory milieu through cell recruitment and cytokine induction. In this work, we specifically propose that CXCL13 contributes to ABMR through two key mechanisms: (1) allowing the spatial and functional integration of Tfh and B cells within TLS to enhance affinity maturation and class switching; and (2) perpetuating a self-sustaining circuit of inflammation and alloantigen recognition that drives sustained donor-specific antibody (DSA) production and endothelial damage.</div><div>The convergence of these mechanisms, driven by the persistent action of CXCL13 within the allograft, could define a new pathophysiological axis in ABMR. Targeting the CXCL13-CXCR5 signaling pathway could represent a promising immunomodulatory strategy to interrupt local humoral amplification, preserve graft integrity, and improve long-term outcomes in kidney transplant recipients.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"206 ","pages":"Article 111842"},"PeriodicalIF":0.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145733767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Immune activation through mimicry of physiological signals: A testable hypothesis on the restoration of surveillance in states of suppression 通过模仿生理信号的免疫激活：在抑制状态下恢复监视的可检验假设

IF 0.8 4区医学

Medical hypotheses Pub Date : 2026-01-01 Epub Date: 2025-12-07 DOI: 10.1016/j.mehy.2025.111848

Murad Novruzov , Marziyya Mammadova , Waseem Ullah Khan , Ulkar Shiraliyeva

{"title":"Immune activation through mimicry of physiological signals: A testable hypothesis on the restoration of surveillance in states of suppression","authors":"Murad Novruzov , Marziyya Mammadova , Waseem Ullah Khan , Ulkar Shiraliyeva","doi":"10.1016/j.mehy.2025.111848","DOIUrl":"10.1016/j.mehy.2025.111848","url":null,"abstract":"<div><div>Profound immune suppression, manifested as anergy, secondary immune dysfunction, or exhaustion, leads to the collapse of immune surveillance in preclinical models of malignancy, sepsis, and chronic viral infection. Existing systemic immunostimulatory approaches are often unable to restore local immune competence without causing off-target inflammation or toxicity. We hypothesize that spatially confined immune reactivation can be achieved by mimicking physiological stimuli through controlled doses and site-specific interventions.</div><div>This concept suggests that immune signaling can be selectively enhanced in target sites by integrating molecular triggers derived from parasitic organisms, mild metabolic stressors such as subtoxic ethanol, and peripheral sensory stimulation. These stimuli are expected to engage conserved neuroimmune and metabolic pathways, promoting localized activation of innate and adaptive immune components.</div><div>The hypothesis remains theoretical and requires confirmation through structured in vitro and in vivo studies. Key risks include allergic sensitization, cytotoxicity, and unintended systemic immune activation. No therapeutic claims are made. The proposed concept offers a testable strategy for restoring immune function in conditions of surveillance system failure and may serve as a basis for future developments of spatially targeted immunomodulators.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"206 ","pages":"Article 111848"},"PeriodicalIF":0.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145733769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Late intraocular lens dislocation arises from two independent biomechanical pathways: Structural failure and interface fatigue 晚期人工晶状体脱位由两种独立的生物力学途径引起：结构破坏和界面疲劳

IF 0.8 4区医学

Medical hypotheses Pub Date : 2026-01-01 Epub Date: 2025-11-24 DOI: 10.1016/j.mehy.2025.111839

Akira Hirata

{"title":"Late intraocular lens dislocation arises from two independent biomechanical pathways: Structural failure and interface fatigue","authors":"Akira Hirata","doi":"10.1016/j.mehy.2025.111839","DOIUrl":"10.1016/j.mehy.2025.111839","url":null,"abstract":"<div><div>Late in-the-bag intraocular lens (IOL) dislocation occurs in 0.1–3 % of patients undergoing cataract surgery, with this prevalence increasing to 15 % in high-risk populations. The current theory attributes all cases to the progressive weakening of zonular fibers, culminating in a single failure mechanism; however, this universal paradigm cannot explain the variety of clinical presentations. This paper proposes that late IOL dislocation results from the failure of a dynamic mechanical system through two independent biomechanical pathways: (1) the structural failure pathway, progressive stiffness reduction through material failure in exfoliation syndrome and dead bag syndrome, and (2) the interface fatigue pathway, repeated cyclic loading causing zonular lamella delamination in post-vitrectomy cases without zonular fiber degradation. Histopathological analysis revealed pathway-specific patterns: all exfoliation syndrome cases (9/9, 100 %) showed zonular fiber rupture, whereas evaluable non-exfoliation cases showed zonular lamella detachment (14/14, 100 % of evaluable cases; 87.5 % of the total 16 non-exfoliation cases); the remaining 2 cases showed dead bag syndrome, where interface assessment was not possible. Temporal patterns were also correlated with exfoliation syndrome cases typically occurring 7–12 years after cataract surgery versus 2–10 years after vitrectomy. When both factors coexist, the risk increases additively, indicating pathway independence. This framework supports pathway-specific interventions, such as capsular tension rings for structural failure and biocompatible vitreous substitutes for dynamic instability, which shift risk stratification from universal protocols to personalized monitoring strategies based on the underlying failure mechanisms.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"206 ","pages":"Article 111839"},"PeriodicalIF":0.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145622317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The brain as curator: A new model of aesthetic cognition 大脑作为策展人：一种新的审美认知模式

IF 0.8 4区医学

Medical hypotheses Pub Date : 2026-01-01 Epub Date: 2025-11-14 DOI: 10.1016/j.mehy.2025.111820

Valentin Skryabin

{"title":"The brain as curator: A new model of aesthetic cognition","authors":"Valentin Skryabin","doi":"10.1016/j.mehy.2025.111820","DOIUrl":"10.1016/j.mehy.2025.111820","url":null,"abstract":"<div><div>Aesthetic experience is often framed as a receptive response to external beauty. This stimulus-centred view understates the mind’s selective labour in converting percepts into meaning. I advance the hypothesis that the brain functions as an internal curator: a control system that confers aesthetic value by sustaining and staging prediction errors at information-dense but tolerable levels instead of eliminating them. Beauty, on this account, arises from curated unpredictability—the controlled violation of expectation that hints at latent structure and is paced toward resolution. Creativity becomes internal exhibition, in which generative and evaluative processes cycle to filter candidate representations in real time. The model yields testable predictions: distinct neural dynamics during active aesthetic choice versus passive exposure; stable individual “curation thresholds” for preferred uncertainty; cultural variation in the staging of deviation; and clinical signatures in depression and mania that reflect failures of selection rather than mood alone. I define curation as a control policy that keeps prediction error near an intermediate, information-maximising level; a simple cost function and two task paradigms make this distinction from precision-weighting testable, enabling falsification via behavioural thresholds (S*), neural coupling signatures during active assembly versus yoked exposure, and clinical sensitivity in depression and mania.</div></div>","PeriodicalId":18425,"journal":{"name":"Medical hypotheses","volume":"206 ","pages":"Article 111820"},"PeriodicalIF":0.8,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145622318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0