Hasil untuk "Neurosciences. Biological psychiatry. Neuropsychiatry"

Xiaoduo Liu, Tao Wei, Bo Zhao et al.

Abstract Background Sleep is essential for brain homeostasis, in part by supporting glymphatic clearance through sleep-related oscillations. However, the relationship between putative glymphatic metrics and coupled sleep rhythm disruption, and their combined role in Alzheimer’s disease (AD) progression, remains poorly understood. Methods We analyzed data from 75 individuals, 54 with AD and 21 cognitively normal (CN) controls, including sleep electroencephalography (EEG), magnetic resonance imaging (MRI), cerebrospinal fluid (CSF) AD biomarkers, and two-year longitudinal cognitive assessments. Putative glymphatic metrics was evaluated using choroid plexus (CP) volume, perivascular spaces (PVSs), diffusion tensor imaging along the perivascular space (DTI-ALPS) index, and blood oxygen level-dependent signal coupled to CSF signal (BOLD-CSF coupling). Coupled sleep rhythm was assessed via slow oscillation (SO)-theta and SO-spindle couplings. Correlation and mediation analyses explored associations between these MRI-derived indices and coupled sleep oscillations, and least absolute shrinkage and selection operator (LASSO) regression was used to predict AD progression. Results Compared to CN controls, individuals with AD had reduced DTI-ALPS index and BOLD-CSF coupling (p < 0.05), along with disrupted SO-spindle coupling (p = 0.029). Across all participants, lower global BOLD-CSF coupling correlated with misaligned SO-theta burst coupling (r = 0.311, p = 0.018), and reduced DTI-ALPS was associated with misaligned SO-spindle coupling (r = 0.370, p = 0.008). In the AD group, DTI-ALPS remained correlated with SO-spindle misalignment (r = 0.376, p = 0.028). Mediation analysis revealed that SO-spindle misalignment contributed to cognitive decline through its effect on DTI-ALPS. Importantly, combining putative glymphatic and sleep EEG metrics effectively predicted AD progression. Conclusions Our findings suggest that disruptions in surrogates marker of glymphatic clearance and coupled sleep rhythms are jointly associated with AD-related cognitive decline. These metrics offer a promising framework for predicting disease progression and understanding neurodegenerative mechanisms in AD. Graphical Abstract

Azher Arafah, Saima Khatoon, Iyman Rasool et al.

This decade has seen the beginning of ground-breaking conceptual shifts in the research of Alzheimer’s disease (AD), which acknowledges risk elements and the evolving wide spectrum of complicated underlying pathophysiology among the range of diverse neurodegenerative diseases. Significant improvements in diagnosis, treatments, and mitigation of AD are likely to result from the development and application of a comprehensive approach to precision medicine (PM), as is the case with several other diseases. This strategy will probably be based on the achievements made in more sophisticated research areas, including cancer. PM will require the direct integration of neurology, neuroscience, and psychiatry into a paradigm of the healthcare field that turns away from the isolated method. PM is biomarker-guided treatment at a systems level that incorporates findings of the thorough pathophysiology of neurodegenerative disorders as well as methodological developments. Comprehensive examination and categorization of interrelated and convergent disease processes, an explanation of the genomic and epigenetic drivers, a description of the spatial and temporal paths of natural history, biological markers, and risk markers, as well as aspects about the regulation, and the ethical, governmental, and sociocultural repercussions of findings at a subclinical level all require clarification and realistic execution. Advances toward a comprehensive systems-based approach to PM may finally usher in a new era of scientific and technical achievement that will help to end the complications of AD.

Md. Adil Faizan, V. Murali Krishna, Tialam Gautham et al.

Background: Mental illness continues to be a significant public health challenge, with stigma acting as a barrier to seeking care and improving outcomes. Healthcare students, particularly medical and nursing students, play an influential role in shaping future societal attitudes toward mental health. Their attitudes and perceptions toward mental illness can directly impact the care patients receive and influence how mental health issues are addressed within the healthcare system. Stigma among healthcare students can undermine the quality of patient care, discourage individuals from seeking help, and perpetuate harmful stereotypes that affect wider societal views. This study compares the stigma toward mental illness between medical and nursing students from two educational institutions in Khammam and Warangal, located in Telangana. Telangana was chosen as the study location due to its unique cultural and educational context, which may provide valuable insights into regional variations in stigma and perceptions of mental health. Materials and Methods: A cross-sectional study was conducted with 827 students from private medical college (Khammam) and government medical college (Warangal). The Mental Illness Clinicians’ Attitudes-2 (MICA-2) scale was used for medical students, while the modified MICA-4 scale was employed for nursing students to measure attitudes toward mental illness. In addition, sociodemographic data, including gender, previous contact with individuals with mental illness, and academic semester, were collected. Results: A total of 827 students participated in the study, with 57.4% of medical students and 42.6% of nursing students. Medical students exhibited significantly higher stigma scores (41.07 ± 6.74) compared to nursing students (38.07 ± 7.44, P < 0.001). Male students had higher stigma levels (41.37 ± 7.06) than female students (36.57 ± 7.33, P < 0.001). Students with prior contact with individuals suffering from mental illness showed lower stigma scores (35.42 ± 8.91) compared to those without prior contact (39.35 ± 6.14, P < 0.001). Students from Warangal had lower stigma scores (38.13 ± 7.03) compared to those from Khammam (39.15 ± 6.54, P < 0.05). Post hoc analysis revealed that medical students from private medical college, Khammam (MedKh) had the highest stigma, followed by nursing students from the same institution. Students from government medical college, Warangal (MedWar) exhibited intermediate stigma, with Government nursing college, Warangal (NurWar) showing the lowest stigma levels. Conclusion: This study highlights significant differences in stigma levels between students from various institutions and regions, emphasizing the importance of addressing stigma in healthcare education. To reduce stigma, it is crucial to integrate anti-stigma programs into medical and nursing curricula, with a focus on mental health awareness. In addition, increasing clinical exposure to mental health settings and fostering direct interaction with individuals experiencing mental illness can help reduce prejudice and promote more compassionate care. These actionable steps can support the development of a more empathetic and stigma-free healthcare workforce.

Michelle Chang

Luciana Cristina Mancio Balico, Gabrielle Siota Schramm, Eduarda Taube Rotta et al.

ABSTRACT Introduction This study explores the associations between Adverse Childhood Experiences (ACEs) and child health in Brazil using data from the PEARLS-BR study. It aims to assess the prevalence and impact of ACEs in a Brazilian cultural context and their relationship with health outcomes. Methods A cross-sectional study was conducted at a Multidisciplinary Health Care Clinical Center and a General Hospital - Reference Center for Child and Adolescent Care, involving 202 caregivers of children and teens aged 0 to 18 years. The PEARLS-BR instrument was used to document the frequency and distribution of ACEs and related life events and their association with health outcomes. Results Caregivers participants reported a median of 2 (IQR 1-5) adversities of their child, with 78.2% reporting at least one adversity. Higher PEARLS-BR scores were significantly associated with poorer physical health (OR: 1.18, 95% CI: 1.01–1.38) and mental health (OR: 1.50, 95% CI: 1.33–1.71), ADHD symptoms (OR: 1.21, 95% CI: 1.09–1.37), infections (OR: 1.13, 95% CI: 1.02–1.26), gastrointestinal disorders (OR: 1.26, 95% CI: 1.12–1.43), and headaches/migraines (OR: 1.22, 95% CI: 1.11–1.35). Related life events were linked to higher odds of obesity (OR: 1.37, 95% CI: 1.02–1.88) and atopic conditions (OR: 1.28, 95% CI: 1.01–1.63). Conclusions The PEARLS-BR score identifies children at risk for various adverse health outcomes. The study highlights the need for targeted interventions and comprehensive strategies to address the impact of childhood adversities on health, providing valuable insights for public health strategies and clinical practices in Brazil.

M. P. Stanley, David A. Silbersweig, David L Perez

Dividing the brain-mind into the specialized fields of neurology and psychiatry has produced many granular advantages, but these silos have imposed barriers to comprehensively understanding and contextualizing the fundamentals governing mental life and its maladies. Scientific inquiry into these fundamentals cannot reach its full potential without interdigitating the boundaries of two specialties of the same organ for both scholarship and clinical practice. We propose that to truly integrate disorders of the brain and the mind for research and clinical care, we must carefully reexamine the classification of its disorders (nosology) as an instrument to develop a coherent pathological and psychological framework. We call on professional organizations from neurology, psychiatry, behavioral neurology, neuropsychiatry, neuropsychology, and other relevant subspecialties (eg, geriatric psychiatry) to convene a multidisciplinary task force to define the current classification principles of their subspecialties and work toward developing an integrated nosology. The effect of a shared classification system, which we acknowledge is a difficult proposition philosophically and politically, would have transformative potential across educational, clinical, scientific, programmatic, and sociocultural realms. If accomplished, this initiative would provide a definitive step toward reducing stigma (and promoting reimbursement parity) for the full spectrum of complex brain disorders (regardless of traditional neurologic vs psychiatric conceptualizations).

Q. Huys, M. Paulus

The reliability of neuroscienti fi c measurements is critical to the translation of neuroscienti fi c advances into clinical applications. In recent years, researchers have uncovered substantial limitations in the reliability of many neuroscience, social science, and psychology fi ndings. Shortcomings in the reliability of scienti fi c research have been prominently featured in both scienti fi c publications and the wider press (1,2). Unreliable scienti fi c fi ndings can be identi fi ed by further research, but this involves diverting efforts away from the truly promising research directions. Unreliable or incorrect research results can have long-lasting and pernicious effects on the state of knowledge (3). These fi ndings have subsequently galvanized efforts into understanding the source of unreliable fi ndings and into addressing them, resulting in important changes to sci-enti fi c procedures that aim to ensure improved replicability. This special issue of Biological Psychiatry: Cognitive Neuroscience and Neuroimaging presents the state of the art in a series of articles covering advances in our understanding of reliability relevant to mental health neuroscience research. The topics range from novel methodologies to a focus on analytical and speci fi c issues in particular settings. First, Botvinik-Nezer and Wager (4) focus on reproducibility of neuroimaging, but their insights and lessons apply much more broadly to the fi eld. They describe novel tools and practices to improve reproducibility, i.e., the ability to identify the same set of results using the same analysis methods on the same data. The fact that this is frequently not possible is a major reminder of the challenges ahead and points to the necessity of improving reporting standards, code and data sharing practices, management of computing environments, and analytic fl exibility. They point to a novel form of “ doing ” science, the Psychological Science Accelerator, whereby a global network of laboratories coordinates data collection for democratically selected studies (5), and a novel form of “ doing ” analyses involving diverse analytical approaches involving a multiverse of

Agnes Magyar, Eva Racz, Clara Matesz et al.

Damage to the vestibular sense organs evokes static and dynamic deficits in the eye movements, posture and vegetative functions. After a shorter or longer period of time, the vestibular function is partially or completely restored via a series of processes such as modification in the efficacy of synaptic inputs. As the plasticity of adult central nervous system is associated with the alteration of extracellular matrix, including its condensed form, the perineuronal net, we studied the changes of brevican expression in the perineuronal nets of the superior vestibular nucleus after unilateral labyrinth lesion. Our results demonstrated that the unilateral labyrinth lesion and subsequent compensation are accompanied by the changing of brevican staining pattern in the perineuronal nets of superior vestibular nucleus of the rat. The reduction of brevican in the perineuronal nets of superior vestibular nucleus may contribute to the vestibular plasticity by suspending the non-permissive role of brevican in the restoration of perineuronal net assembly. After a transitory decrease, the brevican expression restored to the control level parallel to the partial restoration of impaired vestibular function. The bilateral changing in the brevican expression supports the involvement of commissural vestibular fibers in the vestibular compensation. All experimental procedures were approved by the ‘University of Debrecen – Committee of Animal Welfare’ (approval No. 6/2017/DEMAB) and the ‘Scientific Ethics Committee of Animal Experimentation’ (approval No. HB/06/ÉLB/2270-10/2017; approved on June 6, 2017).

Satish Khadilkar, Mehul Desai

Oleksii Eroshkin, Anastasiia Omelchenko, Dmytro Romanukha

Duohao Wang, Qun Yao, Xingjian Lin et al.

PurposeTo explore changes in the brain structural network in patients with cerebellar infarction on different sides and their correlations with changes in cognitive function.MethodsNineteen patients with acute left posterior cerebellar infarction and 18 patients with acute right posterior cerebellar infarction seen from July 2016 to September 2019 in the Department of Neurology, Affiliated Brain Hospital of Nanjing Medical University, were selected. A total of 27 healthy controls matched for sex, age, and years of education were recruited. The subjects underwent head diffusion magnetic resonance imaging examination and neuropsychological cognitive scale evaluation, and we analyzed changes in brain structural network properties in patients with cerebellar infarction and their correlation with changes in patients' cognitive function.ResultsThe Mini-Mental Status Examination (MMSE), Montreal Cognitive Assessment (MOCA) and the Rey auditory verbal learning test (RAVLT) scores in the left and right cerebellar infarction groups were significantly lower than those in the healthy control group (p &lt; 0.05). In addition, the digit span test (DST) scores were lower in the left cerebellar infarction group (p &lt; 0.05); the trail-making test (TMT) times in the right cerebellar infarction group were significantly higher than those in the left cerebellar infarction group (p &lt; 0.05). Meanwhile, the left and right cerebellar infarction groups had abnormal brain topological properties, including clustering coefficient, shortest path length, global efficiency, local efficiency and nodal efficiency. After unilateral cerebellar infarction, bilateral cerebral nodal efficiency was abnormal. Correlation analysis showed that there was a close correlation between decreased processing speed in patients with left cerebellar infarction and decreased efficiency of right cerebral nodes (p &lt; 0.05), and there was a close relationship between executive dysfunction and decreased efficiency of left cerebral nodes in patients with right cerebellar infarction (p &lt; 0.05).ConclusionPatients with cerebellar infarction have cognitive impairment. Unilateral cerebellar infarction can reduce the network efficiency of key regions in the bilateral cerebral hemispheres, and these abnormal changes are closely related to patient cognitive impairment. The results of this study provide evidence for understanding the underlying neural mechanisms of cerebellar cognitive impairment and suggest that brain topological network properties may be markers of cerebellar cognitive impairment.

Han Chen, Xiao-Fen Zhou, Da-Wei Zhou et al.

Abstract Background To evaluate the impact of positive end-expiratory pressure (PEEP) on intracranial pressure (ICP) in animals with different respiratory mechanics, baseline ICP and volume status. Methods A total of 50 male adult Bama miniature pigs were involved in four different protocols (n = 20, 12, 12, and 6, respectively). Under the monitoring of ICP, brain tissue oxygen tension and hemodynamical parameters, PEEP was applied in increments of 5 cm H2O from 5 to 25 cm H2O. Measurements were taken in pigs with normal ICP and normovolemia (Series I), or with intracranial hypertension (via inflating intracranial balloon catheter) and normovolemia (Series II), or with intracranial hypertension and hypovolemia (via exsanguination) (Series III). Pigs randomized to the control group received only hydrochloride instillation while the intervention group received additional chest wall strapping. Common carotid arterial blood flow before and after exsanguination at each PEEP level was measured in pigs with intracranial hypertension and chest wall strapping (Series IV). Results ICP was elevated by increased PEEP in both normal ICP and intracranial hypertension conditions in animals with normal blood volume, while resulted in decreased ICP with PEEP increments in animals with hypovolemia. Increasing PEEP resulted in a decrease in brain tissue oxygen tension in both normovolemic and hypovolemic conditions. The impacts of PEEP on hemodynamical parameters, ICP and brain tissue oxygen tension became more evident with increased chest wall elastance. Compare to normovolemic condition, common carotid arterial blood flow was further lowered when PEEP was raised in the condition of hypovolemia. Conclusions The impacts of PEEP on ICP and cerebral oxygenation are determined by both volume status and respiratory mechanics. Potential conditions that may increase chest wall elastance should also be ruled out to avoid the deleterious effects of PEEP.

N. Yahata, K. Kasai, M. Kawato

R. Novaes, A. Teixeira, A. D. de Miranda

Institute of Biomedical Sciences, Federal University of Alfenas, Alfenas, 37130-001 Minas Gerais, Brazil Department of Structural Biology, Federal University of Alfenas, Alfenas, 37130-001 Minas Gerais, Brazil Neuropsychiatry Program, Department of Psychiatry & Behavioral Sciences, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, USA Interdisciplinary Laboratory of Medical Investigation, School of Medicine, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil Laboratory of Neurobiology, Institute of Biological Sciences, Department of Morphology, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil

Haruo Nishijima, Fumiaki Mori, Akira Arai et al.

Levo-dihydroxyphenylalanine (L-DOPA) is the most effective treatment for Parkinson's disease; however, most patients develop uncontrollable abnormal involuntary movements known as L-DOPA-induced dyskinesia. L-DOPA-induced dyskinesia can be reduced by pallidotomy of the medial globus pallidus or pallidal deep brain stimulation, suggesting that the medial globus pallidus plays a significant role in the development of L-DOPA-induced dyskinesia. In the present study, the pathological changes of the medial globus pallidus in L-DOPA-induced dyskinesia were studied in rat models of Parkinson's disease (unilateral 6-hydroxydopamine lesioning) and L-DOPA-induced dyskinesia (L-DOPA injection in Parkinson's disease-model rats twice daily for 2 weeks, confirmed by display of dyskinesia-like abnormal involuntary movements). L-DOPA-induced dyskinesia-model rats displayed medial globus pallidus hypertrophy, enlarged axon terminals surrounding the dendrites of medial globus pallidus neurons, and increased density of synaptic vesicles in enlarged axon terminals on the lesioned side. Synaptic terminal enlargement reversed after discontinuation of L-DOPA. Histological studies revealed the enlarged synaptic terminals were those of GABAergic striatal (direct pathway) neurons. A single injection of L-DOPA enhanced GABA release in the medial globus pallidus on the lesioned side in L-DOPA-induced dyskinesia-model rats compared to Parkinson's disease-model rats. In addition, microinjection of muscimol, a GABAA receptor agonist, into the medial globus pallidus on the lesioned side of Parkinson's disease-model rats induced dyskinesia-like abnormal involuntary movements. Microinjection of bicuculline, a GABAA receptor antagonist, into the medial globus pallidus on the lesioned side alleviated L-DOPA-induced dyskinesia in Parkinson's disease-model rats that had received L-DOPA prior to the microinjection. These results indicate that priming for L-DOPA-induced dyskinesia comprises excessive GABA storage in axon terminals of the direct pathway and that expression of L-DOPA-induced dyskinesia is associated with enhanced GABA release into the medial globus pallidus after L-DOPA dosing and the resultant excessive stimulation of GABAA receptors.

Jin Zhang, Hui Sang, Xin Zhang et al.

Objective: To study the characteristics and risk factors of carotid atherosclerosis in populations at high risk of stroke in urban and rural areas of North China.Methods: A cross-sectional study was conducted to investigate high stroke risk populations in representative urban and rural areas sampled from 12 regions of China. A pre-designed questionnaire, ultrasound, and laboratory examinations were performed to evaluate risk factors.Results: A total of 30,175 patients were included in the study. The overall prevalence of carotid atherosclerosis was 54.53%, among which intimal thickening and plaque were 39.22 and 41.25%, respectively. The prevalence of carotid atherosclerosis in the urban group was higher than in the rural group. Multivariate logistic regression analysis revealed that male gender, age, smoking, hypertension, dyslipidemia, stroke, atrial fibrillation, systolic blood pressure, and levels of fasting blood glucose, total cholesterol, and low-density lipoprotein cholesterol were the common independent risk factors for carotid atherosclerosis in both groups. Higher education, high salt consumption, passive smoking, family history of stroke, and transient ischemic attack were unique independent risk factors, and high-density lipoprotein cholesterol was a protective factor for carotid atherosclerosis in the urban population.Conclusion: This study suggests that risk factors for carotid atherosclerosis differ between urban and rural populations in North China.

Samuel Chiquita, Elisa J. Campos, João Castelhano et al.

Abstract Background It has been claimed that the retina can be used as a window to study brain disorders. However, concerning Alzheimer’s disease (AD), it still remains controversial whether changes occurring in the brain and retina are associated. We aim to understand when changes start appearing in the retina and brain, how changes progress, and if they are correlated. Methods We carried out a unique longitudinal study, at 4, 8, 12, and 16 months of age, in a triple transgenic mouse model of AD (3×Tg-AD), which mimics pathological and neurobehavioral features of AD, as we have already shown. Retinal structure and physiology were evaluated in vivo using optical coherence tomography and electroretinography. Brain visual cortex structure was evaluated in vivo using magnetic resonance imaging. Results The retinal thickness of 3×Tg-AD decreased, at all time points, except for the outer nuclear layer, where the opposite alteration was observed. Amplitudes in scotopic and photopic responses were increased throughout the study. Similarly, higher amplitude and lower phase values were observed in the photopic flicker response. No differences were found in the activity of retinal ganglion cells. Visual cortex gray matter volume was significantly reduced. Conclusions Our results show that this animal model shows similar neural changes in the retina and brain visual cortex, i.e., retinal and brain thinning. Moreover, since similar changes occur in the retina and brain visual cortex, these observations support the possibility of using the eye as an additional tool (noninvasive) for early AD diagnosis and therapeutic monitoring.

Zareen Amtul, Jun Yang, Ting-Yim Lee et al.

Aberrations in brain microcirculation and the associated increase in blood-brain-barrier (BBB) permeability in addition to neuroinflammation and Aβ deposition observed in Alzheimer’s disease (AD) and ischemia have gained considerable attention recently. However, the role of microvascular homeostasis as a pathogenic substrate to disturbed microperfusion as well as an overlapping etiologic mechanism between AD and ischemia has not been thoroughly explored. In this study, we employ temporal histopathology of cerebral vasculature in a rat model of β-amyloid (Aβ) toxicity and endothelin-1 induced-ischemia (ET1) to investigate the panorama of cerebral pathology and the protein expression on d1, d7, and d28 post-injury. The combination of Aβ and ET1 pathological states leads to an alteration in microvascular anatomy, texture, diameter, density, and protein expression, in addition to disturbed vessel-matrix-connections, inter-compartmental water exchange and basement membrane profile within the lesion epicenter localized in the striatum of Aβ+ET1 brains compared to Aβ and ET1 rats. We conclude that the neural microvascular network, in addition to the neural tissue, is not only sensitive to structural deterioration but also serves as an underlying vascular etiology between ischemia and AD pathologies. Such investigation can provide prospects to appreciate the interrelationships between structure and responses of cerebral microvasculature and to provide a venue for vascular remodeling as a new treatment strategy.

J. van den Stock, F. Kumfor

Jan Van den Stock a,b,c,* and Fiona Kumfor d,e,f a Laboratory for Translational Neuropsychiatry, Department of Neurosciences, KU Leuven, Belgium b Old Age Psychiatry, University Psychiatric Center KU Leuven, Leuven, Belgium c Brain and Emotion Laboratory, Department of Cognitive Neuroscience, Maastricht University, Maastricht, The Netherlands d School of Psychology, The University of Sydney, Sydney, NSW, Australia e Brain & Mind Centre, The University of Sydney, Sydney, NSW, Australia f ARC Centre of Excellence in Cognition and Its Disorders, The University of Sydney, Sydney, NSW, Australia

M. Vargas