Hasil untuk "Neurosciences. Biological psychiatry. Neuropsychiatry"

Yingli Gu, Kijung Sung, Chengbiao Wu

Human-Friedrich Unterrainer, Human-Friedrich Unterrainer, Human-Friedrich Unterrainer et al.

Oceanic states of consciousness—characterized by ego dissolution, unity, and timelessness—have long occupied a liminal space between psychopathology and transcendence. This paper explores these states through the interdisciplinary lens of existential neuroscience, integrating insights from psychoanalysis, existentialism, affective neuroscience, and psychedelic research. Starting with the psychoanalytic tension between Freud’s view of the oceanic feeling as a regressive illusion and Jung’s framing of it as a transformative encounter with the unconscious, this paper examines how creative and mystical experiences often arise from this dissolution of self-boundaries. Drawing on art theorist Anton Ehrenzweig and examples from figures like Vincent van Gogh and Antonin Artaud, I highlight how oceanic states may catalyze both visionary insight and psychological disintegration. Neuroscientific models, including the REBUS theory and studies of the Default Mode Network (DMN), suggest that ego dissolution reflects a flexible reorganization of brain function rather than dysfunction. The Peri-Aqueductal Gray (PAG), a midbrain structure associated with affect regulation and spiritual experience, emerges as a key neural hub linking primal affective states with mystical awareness. Existential thinkers such as Sartre, Heidegger, and Merleau-Ponty provide a philosophical framework for interpreting these phenomena as moments of existential rupture and potential authenticity. Oceanic states thus challenge conventional notions of the self as fixed and bounded. Rather than categorizing them as pathological or purely mystical, it is proposed here that these states represent affectively charged boundary experiences - ones that require contextual integration and offer deep insight into the nature of selfhood, meaning, and transformation.

Hangeul Park, Woojin Kim, Jungbo Sim et al.

Objective Motor-evoked potential (MEP) loss during intramedullary (IM) spinal cord tumor surgery impairs the ability to monitor further neural injury. Direct wave (D-wave) monitoring may allow continued assessment of corticospinal tract integrity after MEP loss. This study evaluates the role of D-wave-guided surgery in preserving function and enabling safe resection after MEP loss. Methods A retrospective study was conducted in adult patients with ependymoma (EPN), cavernous angioma (CA) or subependymoma who experienced MEP loss during IM tumor resection between January 2012 and May 2025. Patients who underwent continued resection under D-wave guidance after MEP loss were compared with those who did not. Results Among 37 eligible patients, 9 underwent D-wave-guided surgery and 28 did not. Functional improvement at the last follow-up was more frequent in the D-wave-guided surgery group (66.7% vs. 17.9%, p=0.011). This trend remained significant in EPN patients (74.4% vs. 9.1%, p=0.003), but not in CA patients. Immediate postoperative motor grade ≤3 was more common in the D-wave-guided surgery group (66.7% vs. 39.3%), although this difference was not statistically significant (p=0.251). By last follow-up, the proportions of patients self-ambulatory without external aids (88.9% vs. 89.3%, p=1.000) were similar between groups. Extent of resection, complications, and recurrence rates showed no significant differences. Conclusion D-wave-guided surgery may enable safe continuation of tumor resection after MEP loss without increasing morbidity. It offers a viable intraoperative strategy to preserve long-term motor function by extending monitoring beyond MEP limitations.

Claudio Singh Solorzano, Marta Spinoni, Maria Grazia Di Benedetto et al.

Objective: An emerging marker of depression in the perinatal period is represented by a reduction in the autonomic nervous system (ANS) activity, reflected by heart rate variability (HRV). This scoping review aims to map the association between HRV and depression during the perinatal period and to understand its potential clinical implications. Introduction: Previous evidence associated ANS dysfunction and depressive symptomatology in the general population. Few observational and intervention studies investigated how HRV could be related to both pre- and post-partum depressive symptoms. However, high heterogeneity in the study designs and methods has been reported. Therefore, this scoping review plans to combine all these findings to build a starting point for future research. Inclusion criteria: This scoping review will consider articles focusing on the association between HRV and depression in the peripartum and – when available – on the impact of interventions on HRV and how this correlates with changes in depressive symptoms. Studies will be included with no restrictions on participants’ age, peripartum time points for the assessment, and HRV parameters collected. Methods: We will perform a systematic search using the Medline (PubMed), PsychInfo, and Web of Science (WoS) databases. Two authors will independently screen titles, abstracts, and then full-text articles that meet the inclusion criteria. The review will include only journal articles published in English, with no time limitations. Data will be extracted and presented in tables and/or graphical representations to summarise and describe the results. Extracted data will be reported in a comprehensive summary.

Nader Fallah, Nader Fallah, Vanessa K. Noonan et al.

Vanessa Kellermann, Ece Sengun Filiz, Olena Said et al.

Abstract Background The OPEN feasibility trial testing olanzapine in anorexia nervosa (AN) in young people (YP) was not successful due to poor recruitment. This study aims to understand clinicians’ views and experiences of using olanzapine in AN and the challenges in implementing the trial in National Health Service (NHS) clinical settings. Methods We conducted qualitative interviews with eating disorders (ED) clinicians involved with the study (n = 11). Framework analysis was applied to qualitative data to identify barriers and facilitators to recruitment and study implementation. A web-based semi-structured Qualtrics survey was administered to ED clinicians (n = 24). Findings from the survey were used to corroborate and expand on the information derived from qualitative interviews. Results Qualitative analysis identified four main themes: (1) Acknowledging Service User (SU) / Family Concerns, (2) Prioritising person-centred care, (3) Limited Service Capacity and (4) Study eligibility criteria. Subthemes are outlined accordingly. Clinicians appeared confident addressing SU concerns around olanzapine in clinical discussions, but timing was critical, and olanzapine was considered one aspect of treatment that needed to align with their holistic approach. Service pressures restricted opportunities for recruitment and the ability to offer regular review. At the same time, some YP were ineligible for the trial, as they were already taking olanzapine, or needed to be prescribed it more promptly than the study procedures allowed. Survey findings underlined confidence in prescribing and informing on olanzapine, the various possible benefits of olanzapine besides weight gain, and the importance of therapeutic alliances and informed consent. Both data sets highlight the need for further evidence on long-term safety, side effects and efficacy of olanzapine use for AN. Where clinical service capacity is at a premium, research implementation is not prioritised, particularly in intensive clinical settings. Conclusions Findings provide first-hand insight into individual and systemic challenges with research implementation in the NHS, which need to be considered when designing future clinical research studies. We emphasise a person-centred approach when discussing olanzapine to consider a holistic recovery from AN beyond weight-gain as an isolated outcome for improvement.

Yuan Cai, Bonnie Y.K. Lam, Xiang Fan et al.

Introduction: Alzheimer's disease-resemblance atrophy index (AD-RAI) is a machine-learning derived MRI-based brain atrophy biomarker that is valid in predicting cognitive decline in subjects with AD. We investigated the performance of AD-RAI in predicting long-term cognitive decline in subjects with stroke or transient ischemic attack (TIA). Methods: We recruited consecutive dementia-free stroke/TIA subjects who had brain MRI at baseline (i.e., within 3-6 months after the index event) and cognitive data at both baseline and 3 years. We defined cognitive decline as an increase in clinical dementia rating scale from 0 to 0.5 or above or from 0.5 to 1 or above at 3 years when compared with baseline. We investigated the association between AD-RAI, traditional brain atrophy biomarkers (hippocampus volume [HV], hippocampal fraction [HF], total brain volume [TBV], TBV/intracranial volume [ICV] ratio, ventricular-brain-ratio, presence of medial temporal lobe atrophy [MTLA]), and cerebral small vessel disease biomarkers (white matter hyperintensity [WMH]) volume, WMHV/ICV ratio presence of confluent WMH, presence of >/=3 lacunes) with cognitive decline. Results: Of 231 participants (mean age 66.0 ± 10.9, 124 [53.7] male), 55(23.8) had cognitive decline at 3 years. Among all the imaging biomarkers, AD-RAI and HV were associated with cognitive decline in univariate regression. Such a relationship was still significant with AD-RAI after adjusted for age, gender, and education (aOR [95%CI] 3.900 [1.221-12.458]). Among all imaging biomarkers, only AD-RAI was associated with slope of Montreal cognitive assessment (MoCA) after adjusted to age, gender, education (β(SE) −0.742[0.242], p=0.002). Discussion: AD-RAI predicted long term cognitive decline in subjects with stroke/TIA.

Abhay Matkar

Seoyeon Won, Jeongyeon An, Hwayoung Song et al.

Currently, neurointervention, surgery, medication, and central nervous system (CNS) stimulation are the main treatments used in CNS diseases. These approaches are used to overcome the blood brain barrier (BBB), but they have limitations that necessitate the development of targeted delivery methods. Thus, recent research has focused on spatiotemporally direct and indirect targeted delivery methods because they decrease the effect on nontarget cells, thus minimizing side effects and increasing the patient’s quality of life. Methods that enable therapeutics to be directly passed through the BBB to facilitate delivery to target cells include the use of nanomedicine (nanoparticles and extracellular vesicles), and magnetic field-mediated delivery. Nanoparticles are divided into organic, inorganic types depending on their outer shell composition. Extracellular vesicles consist of apoptotic bodies, microvesicles, and exosomes. Magnetic field-mediated delivery methods include magnetic field-mediated passive/actively-assisted navigation, magnetotactic bacteria, magnetic resonance navigation, and magnetic nanobots—in developmental chronological order of when they were developed. Indirect methods increase the BBB permeability, allowing therapeutics to reach the CNS, and include chemical delivery and mechanical delivery (focused ultrasound and LASER therapy). Chemical methods (chemical permeation enhancers) include mannitol, a prevalent BBB permeabilizer, and other chemicals—bradykinin and 1-O-pentylglycerol—to resolve the limitations of mannitol. Focused ultrasound is in either high intensity or low intensity. LASER therapies includes three types: laser interstitial therapy, photodynamic therapy, and photobiomodulation therapy. The combination of direct and indirect methods is not as common as their individual use but represents an area for further research in the field. This review aims to analyze the advantages and disadvantages of these methods, describe the combined use of direct and indirect deliveries, and provide the future prospects of each targeted delivery method. We conclude that the most promising method is the nose-to-CNS delivery of hybrid nanomedicine, multiple combination of organic, inorganic nanoparticles and exosomes, via magnetic resonance navigation following preconditioning treatment with photobiomodulation therapy or focused ultrasound in low intensity as a strategy for differentiating this review from others on targeted CNS delivery; however, additional studies are needed to demonstrate the application of this approach in more complex in vivo pathways.

Sapna Erat Sreedharan, K Arun, Santhosh Kannath et al.

Background: Timely and effective recanalization to salvage the penumbra is the main determinant of outcome in acute ischemic strokes. Randomized controlled trials on late window mechanical thrombectomy (MT) have proved its safety and efficacy upto 24 h after stroke onset. We looked at the impact of time to reperfusion on vessel recanalization rates and short-term outcome in patients undergoing MT for large vessel occlusion. Methods: The clinical, imaging, and outcome of all patients undergoing MT upto 24 h from last seen normal was extracted from a prospectively maintained ischemic stroke database from January 2012 till September 2019. Results: There were 145 patients with a mean (SD) age of 58.2 (±14) years. Of them, 28 had wake up/unknown time of onset stroke and 9 presented beyond >360 min. There were 23 vertebrobasilar strokes. Median National Institute of Health Stroke scale score (NIHSS) at admission was 16.4 (Inter quartile range (IQR) 12–21). CT-Alberta Stroke program early CT score (CT-ASPECTS) was excellent (8–10) in 39 (31.6%) and fair (5–7) in 77 (63.6%) patients in anterior circulation strokes. About 25% underwent bridging therapy. Recanalization rates did not differ between those presenting early (<6 h) versus wake up strokes and late presenting patients (81.79% vs 71.9%). Symptomatic Intracerebral hemorrhage (ICH) occurred in 5%. At 3 months, excellent outcome (modified rankin scale <2) was observed in 28.9%. While Admission NIHSS remained strong predictor of poor outcome at 3 months, delay in presentation did not impact MT outcome (37.5% vs 45.79% and P = 0.460). Conclusions: The recanalization rates were similar in patients irrespective of the time to reperfusion from stroke onset. The functional outcome was not inferior in late presenters selected by advanced imaging.

Olof Hjorth, Andreas Frick, Malin Gingnell et al.

Abstract Selective serotonin reuptake inhibitors (SSRIs) and internet-based cognitive behavioral therapy (ICBT) are recommended treatments of social anxiety disorder (SAD), and often combined, but their effects on monoaminergic signaling are not well understood. In this multi-tracer positron emission tomography (PET) study, 24 patients with SAD were randomized to treatment with escitalopram+ICBT or placebo+ICBT under double-blind conditions. Before and after 9 weeks of treatment, patients were examined with positron emission tomography and the radioligands [11C]DASB and [11C]PE2I, probing the serotonin (SERT) and dopamine (DAT) transporter proteins respectively. Both treatment combinations resulted in significant improvement as measured by the Liebowitz Social Anxiety Scale (LSAS). At baseline, SERT-DAT co-expression was high and, in the putamen and thalamus, co-expression showed positive associations with symptom severity. SERT-DAT co-expression was also predictive of treatment success, but predictor-outcome associations differed in direction between the treatments. After treatment, average SERT occupancy in the SSRI + ICBT group was >80%, with positive associations between symptom improvement and occupancy in the nucleus accumbens, putamen and anterior cingulate cortex. Following placebo+ICBT, SERT binding increased in the raphe nuclei. DAT binding increased in both groups in limbic and striatal areas, but relations with symptom improvement differed, being negative for SSRI + ICBT and positive for placebo + ICBT. Thus, serotonin-dopamine transporter co-expression exerts influence on symptom severity and remission rate in the treatment of social anxiety disorder. However, the monoamine transporters are modulated in dissimilar ways when cognitive-behavioral treatment is given concomitantly with either SSRI-medication or pill placebo.

Chien-Chin Chen, Chien-Chin Chen, Pei-Chun Chiang et al.

The recent outbreak of coronavirus disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus 2, has become a global threat. Due to neurological manifestations presented throughout the coronavirus disease process, the potential involvement of COVID-19 in central nervous system has attracted considerable attention. Notably, the neurologic system could be widely affected, with various complications such as acute cerebrovascular events, encephalitis, Guillain-Barré syndrome, and acute necrotizing hemorrhagic encephalopathy. However, the risk assessment of exposure to potential biohazards in the context of the COVID-19 pandemic has not been clearly clarified regarding the sampling, preparation, and processing neurological specimens. Further risk managements and implantations are seldom discussed either. This article aims to provide current recommendations and evidence-based reviews on biosafety issues of preparation and processing of cerebrospinal fluid and neurological specimens with potential coronavirus infection from the bedside to the laboratory.

Anna Nolle, Irene van Dijken, Ciril M. Waelti et al.

Glia cells have a crucial role in the central nervous system and are involved in the majority of neurological diseases. While glia isolation techniques are well established for rodent brain, only recent advances in isolating glial cells from human brain enabled analyses of human-specific glial-cell profiles. Immunopanning that is the prospective purification of cells using cell type-specific antibodies, has been successfully established for isolating glial cells from human fetal brain or from tissue obtained during brain surgeries. Here, we describe an immunopanning protocol to acutely isolate glial cells from post-mortem human brain tissue for e.g. transcriptome and proteome analyses. We enriched for microglia, oligodendrocytes and astrocytes from cortical gray matter tissue from three donors. For each enrichment, we assessed the presence of known glia-specific markers at the RNA and protein levels. In this study we show that immunopanning can be employed for acute isolation of glial cells from human post-mortem brain, which allows characterization of glial phenotypes depending on age, disease and brain regions.

A. Todeva-Radneva, R. Paunova, S. Kandilarova et al.

Psychiatric diagnosis has long been perceived as more of an art than a science since its foundations lie within the observation and the self-report of the patients themselves and objective diagnostic biomarkers are lacking. Furthermore, the diagnostic tools in use not only stray away from the conventional medical framework, but also remain invalidated with evidence-based concepts. However, neuroscience as a source of valid objective knowledge has initiated the process of a paradigm shift underlined by the main concept of psychiatric disorders being "brain disorders". It is also a bridge closing the explanatory gap among the different fields of medicine via the translation of knowledge within a multi-disciplinary framework. The contemporary neuroimaging methods such as fMRI provide researchers with an entirely new set of tools to reform the current status quo by creating an opportunity to define and validate objective biomarkers that can be translated into clinical practice. Combining multiple neuroimaging techniques with the knowledge of the role of genetic factors, neurochemical imbalance and neuroinflammatory processes in the etiopathophysiology of psychiatric disorders is a step towards a comprehensive biological explanation of psychiatric disorders and a final differentiation of psychiatry as a well-founded medical science. In addition the neuroscientific knowledge gained thus far suggests a necessity for directional change to exploring multidisciplinary concepts such as multiple causality and dimensionality of psychiatric symptoms and disorders. A concomitant viewpoint transition of the notion of validity in psychiatry with a focus on an integrative validatory approach may facilitate the building of a collaborative bridge above the wall existing between the scientific fields analyzing the mind and those studying the brain.

A. Mirsky

These words of Bruce were exemplified by the McEwen lab as a breeding place of cutting edge ideas allowing students and postdocs to develop their own careers, while at the same time enriching the knowledge-base of the mother lab. This is marked by the impressive family tree of the “McEwenites” shown at the symposia honoring Bruce’s 60th and 80th birthday. His death caused a shockwave of deep sadness; we will tremendously miss our scientific father and friend. Bruce was born in Fort Collins, Colorado, majored in chemistry at Oberlin College, Ohio and received his pH.D. in cell biology at Rockefeller University in 1964, guided by Vincent Allfrey and Alfred Mirsky. After a post-doctoral fellowship at the Institute of Neurobiology, Göteborg Sweden, from 1964 to 1965 with Holger Hydén, he joined in 1966 the Behavioural Neuroscience program led by Neal Miller at Rockefeller University. First in a small lab in the Gasser Hall, so crowded that night shifts were needed to accommodate all students, then to a more spacious environment in Smith Hall and finally the past decades to the Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology ruling the world from the 13th floor of the Weiss building. In 1968, Bruce discovered that the glucocorticoid stress hormone targets in particular the hippocampus. This key discovery was one of the pillars for the new field of Psychoneuroendocrinology. He showed that stress hormones could act on higher brain regions to promote behavioural adaptation and memory performance. These higher circuits were also target of sex steroids, which explained the molecular basis for the entirely different strategies males and females use to cope with stress. The hormones caused lasting changes in brain development, exerted reversible, activational effects on plasticity and connectivity of the mature neural circuits and could alter the trajectory of neurodegenerative cascades during aging and disease. This research of Bruce served as foundation for the integration of neuroscience and endocrinology with clinical psychology. The 21st century marks Bruce’s leading role in exploring, initially with Eliot Stellar, the overarching concept of allostatic load as calibration of the price the body and brain pay for stress-adaptation. This not only changed the face of psychoneuroendocrine research, but also had social impact which contributed to a better understanding of the link between health and socio-economic status. For instance, in Québec/Canada, universal daycare services at a very low price is offered to families based on the results of studies emerging from the work of Bruce showing that exposure of young children, that live in adversity, to enriched daycare environment can modify the developmental trajectories of the brain and increase resilience later in life. The research of Bruce was recognized with prestigious awards including the Karl Spencer Lashley Award, Pasarow Award in Neuropsychiatry, Goldman-Rakic Prize for Cognitive Neuroscience, Gold Medal from the Society for Biological Psychiatry, the Dale Medal of the British Society for Endocrinology and the Scolnick Prize in Neuroscience. He received the William James Lifetime Achievement Award for Basic Research and the Lifetime Achievement Award of the ISPNE. He was appointed Marius Tausk Visiting Professor in The Netherlands. He was an elected member of the National Academy of Sciences, the National Academy of Medicine, and the American Academy of Arts and Sciences. Public outreach had high priority as was shown by his many media performances. He wrote ‘The End of Stress as We Know It’ with Elizabeth Lasley and the ‘Hostage Brain’, with Harold M. Schmeck jr, in which psychoneuroendocrinology was explained to the lay public. His work was cited more than 130,000 times which ranked him among the top 10 with most impact out of 7 million scientists worldwide. Bruce worked with his wife Karen Bulloch, professor at Rockefeller University, on the immunology of the brain and neurodegenerative diseases. He is survived by his ex-wife Nancy and their two daughters Carolyn and Sarah; with his brother Craig, professor of Sociology at Bowdoin College, Brunswick, he delivered a lecture, recorded as podcast, at University of Pennsylvania on November 21 – the 111th anniversary of their father’s birth. It marked their joint interest in the new

孙萍，聂斌，潘岳松，濮月华，米东华，严鸿伊，龚玲，彭忠勇，刘远亮，刘丽萍

Jie Wang, Jie Wang, Baofeng Yang et al.

BackgroundIn rodents, the period of increased vulnerability to the developmental effects of general anesthetics coincides with the period of age-specific organizing (masculinizing) effects of the major female sex hormone 17β-estradiol (E2) in the male brain and excitatory GABA type A receptor (GABAAR) signaling. We studied whether E2 synthesis and excitatory GABAAR signaling are involved in the mediation of the developmental effects of sevoflurane in male rats.MethodsMale Sprague-Dawley rats were pretreated with the inhibitors of E2 synthesis, formestane, or the Na+-K+-2Cl– (NKCC1) Cl– importer, bumetanide, prior to sevoflurane exposure for 6 h on postnatal (P) day 4, P5, or P6. We tested whether a subsequent exposure of these rats to sevoflurane on P∼10 would cause electroencephalography (EEG)-detectable seizures. We also evaluated their behavior during the elevated plus maze (EPM) test on P∼60, prepulse inhibition (PPI) of acoustic startle responses on P∼70, and corticosterone secretion to physical restraint on P∼80.ResultsThe rats neonatally exposed to sevoflurane responded to repeated exposure to sevoflurane with increased EEG-detectable seizures (F(3,24) = 7.445, P = 0.001) and exhibited deficiencies during the EPM (F(3,55) = 4.397, P = 0.008) and PPI (F(3,110) = 5.222, P = 0.003) tests. They also responded to physical restraint with heightened secretion of corticosterone (F(3,16) = 11.906, P &lt; 0.001). These parameters in the sevoflurane-exposed rats that were pretreated with formestane or bumetanide were not different from those in the control rats.ConclusionThese results, along with previously published data, suggest that sevoflurane-enhanced E2 synthesis and excitatory GABAAR signaling at the time of sevoflurane anesthesia are involved in the mediation of the neurodevelopmental effects of the anesthetic in male rats.

C. Jordan, W. Carlezon

Thalia F. van der Doef, Silvia Zaragoza Domingo, G. Jacobs et al.

Numerous novel neuroscience-based drug targets have been identified in recent years. However, it remains unclear how these targets relate to the expression of symptoms in central nervous system (CNS) disorders in general and psychiatric disorders in particular. To discuss this issue, a New Frontiers Meetings of European College of Neuropsychopharmacology (ECNP) was organized to address the challenges in translational neuroscience research that are impeding the effective development of new treatments. The main aim of this meeting was to discuss scientific insights, concepts and methodologies in order to improve drug development for psychiatric disorders. The meeting was designed to bring together stakeholders from academia, pharmaceutical industry, and regulatory agencies. Here we provide a synopsis of the proceedings from the meeting entitled 'New approaches to psychiatric drug development'. New views on psychiatric drug development were presented to address the challenges and pitfalls as identified by the different stakeholders. The general conclusion of the meeting was that drug discovery could be stimulated by designing new classification and sensitive assessment tools for psychiatric disorders, which bear closer relationships to neuropharmacological and neuroscientific developments. This is in line with the vision of precision psychiatry in which patients are clustered, not merely on symptoms, but primarily on biological phenotypes that represent pathophysiological relevant and 'drugable' processes. To achieve these goals, a closer collaboration between all stakeholders in early stages of development is essential to define the research criteria together and to reach consensus on new quantitative biological methodologies and etiology-directed treatments.