Search

Context: Sports-related concussions are commonly occurring injuries as a result of sports and recreation that may cause alterations in brain functioning. It is important to be able to evaluate the impact of these injuries on function to manage the injury recovery and ensure recovery. Recent literature suggests the use of objective evaluation strategies in a multifaceted approach to evaluate and manage these injuries. It is important to understand the relationships between the assessments and how best to utilize each assessment. The purpose of this study was to investigate if relationships exist between measures of vestibular function at baseline in assessments that may be used following sports-related concussions. Additionally, a secondary purpose was to determine if self-reported symptoms were related to performance on the assessments. This study aimed to identify if these assessments measured independent functions of the vestibulo–ocular reflex or if some redundancy existed among the assessment strategies. Design: A cross-sectional study design was used in a cohort of collegiate athletes ages 18–24. Methods: Participants completed demographics questionnaires, the Post-Concussion Symptom Scale, Gaze Stabilization Test, and Concussion Balance Test. Spearman rho correlations were used to examine the relationships between the measures. Results: One hundred and thirty-five collegiate athletes (82 males and 53 females) were included, representative of 3 sports (cheerleading, soccer, and football) with a mean age of 19.77 (1.42) years old. There were weak to moderate, significant relationships between measures of Gaze Stabilization Test and Concussion Balance Test errors (r =.20–.31, P =.001–.03). Conclusions: The direction of these relationships indicated that greater Concussion Balance Test errors were associated with greater Gaze Stabilization Test performance. These relationships may be attributed to the difficulty created by the foam conditions and the integration of more complex sensory tasks required to maintain balance during the more difficult conditions. [ABSTRACT FROM AUTHOR]

Synapses are fundamental to the function of the central nervous system and are implicated in a number of brain disorders. Despite their pivotal role, a comprehensive imaging resource detailing the distribution of synapses in the human brain has been lacking until now. Here, we employ high-resolution PET neuroimaging in healthy humans (17F/16M) to create a 3D atlas of the synaptic marker Synaptic Vesicle glycoprotein 2A (SV2A). Calibration to absolute density values (pmol/ml) was achieved by leveraging postmortem human brain autoradiography data. The atlas unveils distinctive cortical and subcortical gradients of synapse density that reflect functional topography and hierarchical order from core sensory to higher-order integrative areas-a distribution that diverges from SV2A mRNA patterns. Furthermore, we found a positive association between IQ and SV2A density in several higher-order cortical areas. This new resource will help advance our understanding of brain physiology and the pathogenesis of brain disorders, serving as a pivotal tool for future neuroscience research. [ABSTRACT FROM AUTHOR]

Introduction: Carotid endarterectomy is performed for patients with symptomatic carotid artery occlusions. Surgery can be performed under general and regional anesthesia. Traditionally, surgery is performed under deep cervical plexus block which is technically difficult to perform and can cause serious complications. This case series describes 5 cases in which an intermediate cervical plexus block was used in combination with a superficial cervical plexus block for Carotid endarterectomy surgery. Methods: Five patients who were classified as American Society of Anesthesiologists 2–3 were scheduled for Carotid endarterectomy due to symptoms and more than 70% occlusion of the carotid arteries. The procedures were carried out in the University Teaching Hospital- Peradeniya, Sri Lanka. All patients were given superficial cervical plexus block followed by intermediate cervical plexus block using 2% lignocaine and 0.5% plain bupivacaine. Results: Adequate anesthesia was achieved in 4 patients, and local infiltration was necessary in 1 patient. Two patients developed hoarseness of the voice, which settled 2 h after surgery. Hemodynamic fluctuations were observed in all 5 patients. No serious complications were observed. All 5 patients had uneventful recoveries. Discussions: Regional anesthesia for CEA is preferable in patients who are medically complicated to undergo anesthesia or in patients for whom cerebral monitoring is not available. Intermediate cervical plexus block is described for thyroid surgeries in literature, but not much details on its use for carotid surgeries. Deep cervical plexus blocks has few serious complications which is not there with the use of ICPB making it a good alternative for CEA surgeries. Conclusions: Superficial cervical plexus block and intermediate cervical plexus block can be used effectively for providing anesthesia for patients undergoing Carotid endarterectomy. It is safe and easier to conduct than deep cervical plexus block and enables monitoring of cerebral function. [ABSTRACT FROM AUTHOR]

Gene expression is a critical component of brain physiology, but monitoring this expression in the living brain represents a major challenge. Here, we introduce a new paradigm called recovery of markers through insonation (REMIS) for noninvasive measurement of gene expression in the brain with cell type, spatial, and temporal specificity. Our approach relies on engineered protein markers that are produced in neurons but exit into the brain's interstitium. When ultrasound is applied to targeted brain regions, it opens the blood-brain barrier and releases these markers into the bloodstream. Once in blood, the markers can be readily detected using biochemical techniques. REMIS can noninvasively confirm gene delivery and measure endogenous signaling in specific brain sites through a simple insonation and a subsequent blood test. REMIS is reliable and demonstrated consistent improvement in recovery of markers from the brain into the blood. Overall, this work establishes a noninvasive, spatially specific method of monitoring gene delivery and endogenous signaling in the brain. [ABSTRACT FROM AUTHOR]

Traumatic brain injury (TBI) survivors face debilitating long-term psychosocial consequences, including social isolation and depression. TBI modifies neurovascular physiology and behavior but the chronic physiological implications of altered brain perfusion on social interactions are unknown. Adult C57/BL6 male mice received a moderate cortical TBI, and social behaviors were assessed at baseline, 3-, 7-, 14-, 30-, and 60-days post injury (dpi). Magnetic resonance imaging (MRI, 9.4T) using dynamic susceptibility contrast perfusion weighted MRI were acquired. At 60dpi mice underwent histological angioarchitectural mapping. Analysis utilized standardized protocols followed by cross-correlation metrics. Social behavior deficits at 60dpi emerged as reduced interactions with a familiar cage-mate (partner) that mirrored significant reductions in cerebral blood flow (CBF) at 60dpi. CBF perturbations were dynamic temporally and across brain regions including regions known to regulate social behavior such as hippocampus, hypothalamus, and rhinal cortex. Social isolation in TBI-mice emerged with a significant decline in preference to spend time with a cage mate. Cortical vascular density was also reduced corroborating the decline in brain perfusion and social interactions. Thus, the late emergence of social interaction deficits mirrored the reduced vascular density and CBF in regions known to be involved in social behaviors. Vascular morphology and function improved prior to the late decrements in social function and our correlations strongly implicate a linkage between vascular density, cerebral perfusion, and social interactions. Our study provides a clinically relevant timeline of alterations in social deficits alongside functional vascular recovery that can guide future therapeutics. [ABSTRACT FROM AUTHOR]

Human moral reactions to artificial intelligence (AI) agents' behavior constitute an important aspect of modern-day human–AI relationships. Although previous studies have mainly focused on autonomy ethics, this study investigates how individuals judge AI agents' violations of community ethics (including betrayals and subversions) compared with human violations. Participants' behavioral responses, event-related potentials (ERPs), and individual differences were assessed. Behavioral findings reveal that participants rated AI agents' community-violating actions less morally negative than human transgressions, possibly because AI agents are commonly perceived as having less agency than human adults. The ERP N1 component showed the same pattern with moral rating scores, indicating the modulation effect of human–AI differences on initial moral intuitions. Moreover, the level of social withdrawal correlated with a smaller N1 in the human condition but not in the AI condition. The N2 and P2 components were sensitive to the difference between the loyalty/betrayal and authority/subversion domains but not human/AI differences. Individual levels of moral sense and autistic traits also influenced behavioral data, especially on the loyalty/betrayal domain. In our opinion, these findings offer insights for predicting moral responses to AI agents and guiding ethical AI development aligned with human moral values. [ABSTRACT FROM AUTHOR]

Objective: Early life experiences, including attachment-related experiences, inform internal working models that guide adult relationship behaviors. Few studies have examined the association between adolescent attachment and adult relationship behavior on a neural level. The current study examined attachment in adolescence and its associations with neural correlates of relationship behaviors in adulthood. Method: 85 participants completed the Adult Attachment Interview (AAI) at age 14. Ten years later, at age 24, participants underwent functional brain image when participants were under the threat of electric shock alone, holding the hand of a stranger, or their partner. Results: We found that adolescents who were securely attached at age 14 showed increased activation in regions commonly associated with cognitive, affective, and reward processing when they held the hand of their partner and stranger compared to being alone. Adolescents with higher preoccupied attachment scores showed decreased activation in similar regions only during the stranger handholding condition compared to being alone. Conclusions: These findings suggest that adolescent attachment predicts adult social relationship behaviors on a neural level, in regions largely consistent with previous literature. Broadly, this study has implications for understanding long-term links between attachment and adult relationship behaviors and has potential for informing intervention. [ABSTRACT FROM AUTHOR]

Background: Alcohol is commonly consumed by adolescents in a binge‐like pattern, which can lead to long‐lasting cognitive deficits, including reduced behavioral flexibility. We and others have determined that adolescent intermittent ethanol (AIE) exposure leads to increased number of perineuronal net (PNN) numbers in brain regions that are important for behavioral flexibility. However, whether altered neurochemistry stemming from AIE exposure plays a significant role in reduced behavioral flexibility is unknown. Methods: We measured the number and size of parvalbumin expressing (PV+) interneurons and associated PNNs within the orbitofrontal cortex (OFC), prelimbic cortex (PrL), infralimbic cortex (IL), and anterior insular cortex (AIC) of female and male rats following AIE or control exposure and subsequent training on an attentional set‐shift task (ASST). We then ran analyses to determine whether AIE‐induced changes in PV and PNN measures statistically mediated the AIE‐induced behavioral deficit in reversal learning. Results: We demonstrate that AIE exposure impaired behavioral flexibility on reversal two of the ASST (i.e., recalling the initial learned associations), and led to smaller PV+ cells and increased PNN numbers in the AIC. Interestingly, PNN size and number were not altered in the PrL or IL following AIE exposure, in contrast to prior reports. Mediation analyses suggest that AIE alters behavioral flexibility, at least in part through changes in PV and PNN fluorescent measures in the AIC. Conclusions: This study reveals a significant link between AIE exposure, neural alterations, and diminished behavioral flexibility in rats, and highlights a potential novel mechanism comprising changes in PV and PNN measures within the AIC. Future studies should explore the impact of PNN degradation within the AIC on behavioral flexibility. [ABSTRACT FROM AUTHOR]

Background: Although the World Health Organization recommends visible and clear warning labels about the risks of alcohol consumption on containers and advertising, many of the currently used labels are too small to be visible. This study investigated the brain activity (using fMRI) and alcohol consumption intentions of French young men exposed to two warning formats displayed on alcoholic beverage advertisements: a small Text‐only Alcohol Warning (TAW) currently used in many countries, and a larger text‐and‐picture alcohol warning (PAW). Methods: Seventy‐four eligible 18–25‐year‐old male drinkers completed a face‐to‐face individual visit with a physician expert in addiction medicine. This was followed by the fMRI session during which they viewed 288 stimuli [96 alcohol advertisements with TAWs, the same 96 advertisements with PAWs, and 96 water advertisements (controls)] for 3 s each. If the advertisement made participants want ("yes")/do not want ("no") to consume the product, they pressed the corresponding button (self‐report responses). The number of "yes" responses was compared between advertisement types with a paired sample t‐test. Whole‐brain and region‐of‐interest (ROI) analyses of the fMRI data were performed. Results: Whole‐brain BOLD fMRI highlighted contrasting effects of PAWs and TAWs. Compared with TAWs, PAWs elicited more activation in the precuneus, angular gyrus, occipital, frontal and temporal areas, and less activation in the nucleus accumbens, ventral tegmental areas, and putamen areas (regions of the reward circuit). The ROI analysis confirmed less activation in the reward circuit (left and right ventral tegmental areas, left and right nucleus accumbens) when viewing PAWs than TAWs. Analysis of the self‐report responses indicated that the desire to consume the advertised alcohol product was lower when PAWs were viewed (compared with TAWs) (T = 8.18, p < 10−11). Conclusions: This is the first fMRI study to assess the effect of different alcohol warning formats. Our findings show that compared with TAWs, stronger PAWs in advertisements elicited less activity in key regions of the reward system. This suggests that the effects may influence the desire to consume alcohol products (self‐report response analysis). These results could help policymakers who are interested in developing more effective labeling measures that target young people. [ABSTRACT FROM AUTHOR]

Exportin 1 (XPO1) is the major karyopherin‐β nuclear receptor mediating the nuclear export of hundreds of proteins and some classes of RNA and regulates several critical processes in the cell, including cell‐cycle progression, transcription and translation. Viruses have co‐opted XPO1 to promote nucleocytoplasmic transport of viral proteins and RNA. Maize mosaic virus (MMV) is a plant‐infecting rhabdovirus transmitted in a circulative propagative manner by the corn planthopper, Peregrinus maidis. MMV replicates in the nucleus of plant and insect hosts, and it remains unknown whether MMV co‐opts P. maidis XPO1 (PmXPO1) to complete its life cycle. Because XPO1 plays multiple regulatory roles in cell functions and virus infection, we hypothesized that RNAi‐mediated silencing of XPO1 would negatively affect MMV accumulation and insect physiology. Although PmXPO1 expression was not modulated during MMV infection, PmXPO1 knockdown negatively affected MMV accumulation in P. maidis at 12 and 15 days after microinjection. Likewise, PmXPO1 knockdown negatively affected P. maidis survival and reproduction. PmXPO1 exhibited tissue‐specific expression patterns with higher expression in the ovaries compared with the guts of adult females. Survival rate was significantly lower for PmXPO1 knockdown females, compared with controls, but no effect was observed for males. PmXPO1 knockdown experiments revealed a role for PmXPO1 in ovary function and egg production. Oviposition and egg hatch on plants were dramatically reduced in females treated with dsRNA PmXPO1. These results suggest that PmXPO1 is a positive regulator of P. maidis reproduction and that it plays a proviral role in the insect vector supporting MMV infection. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is one of the most common neurodegenerative diseases, and the most prevalent form of dementia. The main hallmarks for the diagnosis of AD are extracellular amyloid-beta (Aβ) plaque deposition and intracellular accumulation of highly hyperphosphorylated Tau protein as neurofibrillary tangles. The brain consumes more oxygen than any other organs, so it is more easily to be affected by hypoxia. Hypoxia has long been recognized as one of the possible causes of AD and other neurodegenerative diseases, but the exact mechanism has not been clarified. In this review, we will elucidate the connection between hypoxia-inducible factors-1α and AD, including its contribution to AD and its possible protective effects. Additionally, we will discuss the relationship between oxidative stress and AD as evidence show that oxidative stress acts on AD-related pathogenic factors such as mitochondrial dysfunction, Aβ deposition, inflammation, etc. Currently, there is no cure for AD. Given the close association between hypoxia, oxidative stress, and AD, along with current research on the protective effects of antioxidants against AD, we speculate that antioxidants could be a potential therapeutic approach for AD and worth further study. [ABSTRACT FROM AUTHOR]

Despite extensive studies published on the canine brain, inconsistencies and disagreements in the nomenclature and representation of various cerebral structures continue to exist. This study aimed to create a comprehensive mapping of the external architecture of the mesocephalic canine brain with a focus on the major gyri and sulci. Standardized dissection techniques were used on 20 ethically sourced brains obtained from 6 to 10-year-old dogs that were free of neurological disorders. Distinct gyri and sulci with unique locations and bordering structures were observed. Thus, it was possible to identify the often-ignored subprorean gyrus. In addition, this study was able to illustrate the unique locations and bordering structures of gyri and sulci. The findings can contribute to a consensus among researchers on the canine brain anatomy and assist in clarifying the inconsistencies in cerebral structure representation. Furthermore, the results of this study may hold significant implications for veterinary medicine and neuroscience and serve as a foundation for the development of diagnostic and therapeutic approaches for various neurological diseases in dogs. Our findings offer valuable insights into the unique evolutionary adaptations and specialized behaviors of the canine brain, thereby increasing awareness about the neural structures that enable dogs to demonstrate their unique traits. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) and inflammatory bowel disease (IBD) are chronic diseases affecting the central nervous system and gastrointestinal tract, respectively. Recent research suggests a bidirectional relationship between neurodegeneration in PD and intestinal inflammation in IBD. PD patients may experience gastrointestinal dysfunction over a decade before motor symptom onset, and IBD may increase the risk of developing PD. Despite the "gut-brain axis" concept, the underlying pathophysiological mechanisms of this potential association remain unclear. This study aimed to investigate the biological mechanisms of differentially expressed genes in PD and IBD using bioinformatics tools, providing novel insights into the co-diagnosis and treatment of these diseases. We constructed a gene marker for disease diagnosis and identified five important genes (BTK, NCF2, CRH, FCGR3A and SERPINA3). Through nomogram and decision tree analyses, we found that both the IBD and PD required only the expression levels of BTK and NCF2 for accurate discrimination. Additionally, small molecule drugs RO-90-7501 and MST-312 may be useful for the treatment of both IBD and PD. These findings offer new perspectives on the co-diagnosis and treatment of PD and IBD, and suggest that targeting BTK may be a promising therapeutic strategy for both diseases. [ABSTRACT FROM AUTHOR]

The aging population in Canada has been increasing continuously throughout the past decades. Amongst this demographic, around 11% suffer from some form of cognitive decline. While diagnosis through traditional means (i.e., Magnetic Resonance Imagings (MRIs), positron emission tomography (PET) scans, cognitive assessments, etc.) has been successful at detecting this decline, there remains unexplored measures of cognitive health that could reduce stress and cost for the elderly population, including approaches for early detection and preventive methods. Such efforts could additionally contribute to reducing the pressure and stress on the Canadian healthcare system, as well as improve the quality of life of the elderly population. Previous evidence has demonstrated emotional facial expressions being altered in individuals with various cognitive conditions such as dementias, mild cognitive impairment, and geriatric depression. This review highlights the commonalities among these cognitive health conditions, and research behind the contactless assessment methods to monitor the health and cognitive well-being of the elderly population through emotion expression. The contactless detection approach covered by this review includes automated facial expression analysis (AFEA), electroencephalogram (EEG) technologies and heart rate variability (HRV). In conclusion, a discussion of the potentials of the existing technologies and future direction of a novel assessment design through fusion of AFEA, EEG and HRV measures to increase detection of cognitive decline in a contactless and remote manner will be presented. [ABSTRACT FROM AUTHOR]

Introduction: Studies on the aging brain often occur in active settings, but comparatively few investigate brain activity in resting states. However, exploring brain activity in a resting state offers valuable insights into spontaneous neural processes unaffected by task-specific influences. Objective: To investigate the relationship between self-care practices, cognitive function, and patterns of brain activity in healthy older adults, taking into account predictions from aging brain models. Methodology: 77 older adults aged 61 to 87 completing a self-care practices questionnaire, neuropsychological tests, and resting-state electroencephalogram (EEG) recordings. Participants were classified into two groups according to their self-care practices: traditional self-care (T-SC) and developmental self-care (D-SC). Results: Although neuropsychological tests did not yield significant differences between the D-SC and T-SC groups, patterns of brain activity revealed distinct behaviors. The T-SC group demonstrated patterns more consistent with established aging brain models, contrasting with the D-SC group, which exhibited brain activity akin to that observed in younger adults. Specifically, the T-SC group displayed hyperactivation related to memory and executive function performance, alongside heightened alpha power in posterior regions. Furthermore, bilateral frontal activation in the beta band was evident. Conclusions: The findings suggest a nuanced relationship between self-care practices and brain activity in older adults. While the T-SC group demonstrated brain activity patterns consistent with conservative aging, indicating the preservation of typical aging characteristics, the D-SC group displayed activity suggestive of a potential protective effect. This effect may be linked to self-care strategies that foster development and resilience in cognitive aging. [ABSTRACT FROM AUTHOR]

As the most common cause of dementia, Alzheimer's disease (AD) is characterized by neurodegeneration and synaptic loss with an increasing prevalence in the elderly. Increased inflammatory responses triggers brain cells to produce pro-inflammatory cytokines and accelerates the Aβ accumulation, tau protein hyper-phosphorylation leading to neurodegeneration. Therefore, in this paper, we discuss the current understanding of how inflammation affects brain activity to induce AD pathology, the inflammatory biomarkers and possible therapies that combat inflammation for AD. [ABSTRACT FROM AUTHOR]

Introduction: Older adults experience less anxiety. We examined how memory of negative emotional images varied with age and may reflect age-related differences in anxiety. Methods: Fifty-one adults, age 22-80 years, underwent imaging with a memory task where negative and neutral images were displayed pseudo-randomly. They were queried post-scan about the images inter-mixed with an equal number of images never displayed. Sensitivity (d') and reporting bias (Z-score of false alarm rate; Z[FAR]) were quantified with signal detection theory. Results: Age was negatively correlated with both Spielberg State Trait Anxiety Inventory (STAI) state score and d' (negative - neutral) and positively with Z[FAR] (negative - neutral). However, STAI score and d' or Z[FAR] (negative - neutral) were not significantly correlated. In whole-brain regression, STAI score was correlated with higher activity of the right middle/superior temporal gyri/temporal parietal junction (MTG/STG/TPJ) for "negative correct - incorrect" - "neutral correct - incorrect" trials. Further, the MTG/STG/TPJ activity (β) was also negatively correlated with age. Mediation analyses supported a complete mediation model of age → less anxiety → less MTG/STG/TPJ β. Discussion: Together, the findings demonstrated age-related changes in negative emotional memory and how age-related reduction in anxiety is reflected in diminished temporoparietal cortical activities during encoding of negative emotional memory. [ABSTRACT FROM AUTHOR]

Physiotherapists working in hospitals have a key role in decisions about when a person with stroke is safe to walk independently. The aim of this study was to explore the factors influencing decision-making of physiotherapists in this situation. A qualitative design with semi-structured interviews and reflexive thematic analysis was used. Fifteen physiotherapists with recent experience working in inpatient stroke rehabilitation participated. Multiple factors influence decision-making about walking independence after stroke in hospitals. Four themes were identified: (1) Assessment of walking safety involves observation of walking function and consideration of complex individual factors; (2) Perspectives on risk vary, and influence whether a person is considered safe to walk; (3) Institutional culture involves background pressures that may influence decision-making; and (4) Physiotherapists adopt a structured, individualised mobility progression to manage risk. Physiotherapists consistently use observation of walking and understanding of attention and perception in this decision-making. There can sometimes be a conflict between goals of independence and of risk avoidance, and decisions are made by personal judgements. Decision-making about independent walking for people in a hospital after a stroke is complex. Improved guidance about clinical assessment of capacity and determining acceptable risk may enable physiotherapists to engage more in shared decision-making. Regaining independence in walking after a stroke comes with the potential risk of falls. Assessment of walking safety should be specific to the complexity of the situation and consider perception and cognition. Benefits of activity and autonomy, and the risk of falls need to be considered in decisions about walking independence. Patients with the capacity to understand consequences and accept risk can be active participants in determining what is sufficiently safe. [ABSTRACT FROM AUTHOR]

Professor Richard (Rick) Morimoto is the Bill and Gayle Cook Professor of Biology and Director of the Rice Institute for Biomedical Research at Northwestern University. He has made foundational contributions to our understanding of how cells respond to various stresses, and the role played in those responses by chaperones. Working across a variety of experimental models, from C. elegans to human neuronal cells, he has identified a number of important molecular components that sense and respond to stress, and he has dissected how stress alters cellular and organismal physiology. Together with colleagues, Professor Morimoto has coined the term “proteostasis” to signify the homeostatic control of protein expression and function, and in recent years he has been one of the leaders of a consortium trying to understand proteostasis in healthy and disease states. I took the opportunity to talk with Professor Morimoto about proteostasis in general, the aims of the consortium, and how autophagy is playing an important role in their research effort. [ABSTRACT FROM AUTHOR]

Background: Currently, the impact of drug therapies on neurodegenerative conditions is limited. Therefore, there is a strong clinical interest in nonpharmacological interventions aimed at preserving functionality, delaying disease progression, reducing disability, and improving quality of life for both patients and their caregivers. This longitudinal multicenter Randomized Controlled Trial (RCT) applies three innovative cognitive telerehabilitation (TR) methods to evaluate their impact on brain functional connectivity reconfigurations and on the overall level of cognitive and everyday functions. Methods: We will include 110 participants with mild cognitive impairment (MCI). Fifty-five participants will be randomly assigned to the intervention group who will receive cognitive TR via three approaches, namely: (a) Network-based Cognitive Training (NBCT), (b) Home-based Cognitive Rehabilitation (HomeCoRe), or (c) Semantic Memory Rehabilitation Training (SMRT). The control group (n  =  55) will receive an unstructured home-based cognitive stimulation. The rehabilitative program will last either 4 (NBTC) or 6  weeks (HomeCoRe and SMRT), and the control condition will be adapted to each TR intervention. The effects of TR will be tested in terms of Δ connectivity change, obtained from high-density electroencephalogram (HD-EEG) or functional magnetic resonance imaging at rest (rs-fMRI), acquired before (T0) and after (T1) the intervention. All participants will undergo a comprehensive neuropsychological assessment at four timepoints: baseline (T0), within 2  weeks (T1), and after 6 (T2) and 12  months (T3) from the end of TR. Discussion: The results of this RCT will identify a potential association between improvement in performance induced by individual cognitive TR approaches and modulation of resting-state brain connectivity. The knowledge gained with this study might foster the development of novel TR approaches underpinned by established neural mechanisms to be validated and implemented in clinical practice. [ABSTRACT FROM AUTHOR]

Multiple subfields of neuroscience research are beginning to incorporate astrocytes into current frameworks of understanding overall brain physiology, neuronal circuitry, and disease etiology that underlie sleep and sleep-related disorders. Astrocytes have emerged as a dynamic regulator of neuronal activity through control of extracellular space (ECS) volume and composition, both of which can vary dramatically during different levels of sleep and arousal. Astrocytes are also an attractive target of sleep research due to their prominent role in the glymphatic system, a method by which toxic metabolites generated during wakefulness are cleared away. In this review we assess the literature surrounding glial influences on fluctuations in ECS volume and composition across the sleep-wake cycle. We also examine mechanisms of astrocyte volume regulation in glymphatic solute clearance and their role in sleep and wake states. Overall, findings highlight the importance of astrocytes in sleep and sleep research. [ABSTRACT FROM AUTHOR]

Epilepsy is a neurological disorder characterized by recurrent seizures, affecting over 65 million people worldwide. Treatment typically commences with the use of anti-seizure medications, including both mono- and poly-therapy. Should these fail, more invasive therapies such as surgery, electrical stimulation and focal drug delivery are often considered in an attempt to render the person seizure free. Although a significant portion ultimately benefit from these treatment options, treatment responses often fluctuate over time. The physiological mechanisms underlying these temporal variations are poorly understood, making prognosis a significant challenge when treating epilepsy. Here we use a dynamic network model of seizure transition to understand how seizure propensity may vary over time as a consequence of changes in excitability. Through computer simulations, we explore the relationship between the impact of treatment on dynamic network properties and their vulnerability over time that permit a return to states of high seizure propensity. For small networks we show vulnerability can be fully characterised by the size of the first transitive component (FTC). For larger networks, we find measures of network efficiency, incoherence and heterogeneity (degree variance) correlate with robustness of networks to increasing excitability. These results provide a set of potential prognostic markers for therapeutic interventions in epilepsy. Such markers could be used to support the development of personalized treatment strategies, ultimately contributing to understanding of long-term seizure freedom. [ABSTRACT FROM AUTHOR]

Background: A major risk factor for neurodegenerative disorders is old age. Nutritional interventions that delay aging, such as calorie restriction (CR) and intermittent fasting (IF), as well as pharmaceuticals that affect the pathways linking nutrition and aging processes, have been developed in recent decades and have been shown to alleviate the effects of aging on the brain. Summary: CR is accomplished by alternating periods of ad libitum feeding and fasting. In animal models, IF has been shown to increase lifespan and slow the progression and severity of age-related pathologies such as cardiovascular and neurodegenerative diseases and cancer. According to recent research, dietary changes can help older people with dementia retain brain function. However, the mechanisms underlying the neuroprotective effect of IF on the aging brain and related questions in this area of study (i.e., the potential of IF to treat neurodegenerative disorders) remain to be examined. Key Messages: This review addresses the hypothesis that IF may have translational potential in protecting the aged brain while summarizing the research supporting the putative neuroprotective mechanisms of IF in animal models. Additionally, given the emerging understanding of the connection between aging and dementia, our investigations may offer a fresh perspective on the use of dietary interventions for enhancing brain function and preventing dementia in elderly individuals. Finally, the absence of guidelines regarding the application of IF in patients hampers its broad utilization in clinical practice, and further studies are needed to improve our knowledge of the long-term effects of IF on dementia before it can be widely prescribed. In conclusion, IF may be an ancillary intervention for preserving memory and cognition in elderly individuals. [ABSTRACT FROM AUTHOR]

Purpose This study aimed to develop a normal brain ageing model based on magnetic resonance imaging and radiomics, therefore identifying radscore, an imaging indicator representing white matter heterogeneity and exploring the significance of radscore in detecting people's cognitive changes. Methods Three hundred sixty cognitively normal (CN) subjects from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database and 105 CN subjects from the Parkinson's Progression Markers Initiative database were used to develop the model. In ADNI, 230 mild cognitive impairment (MCI) subjects were matched with 230 CN old-aged subjects to evaluate their heterogeneity difference. One hundred four MCI subjects with 48 months of follow-up were divided into low and high heterogeneity groups. Kaplan–Meier survival curve analysis was used to observe the importance of heterogeneity results for predicting MCI progression. Results The area under the receiver operating characteristic curve of the model in the training, internal test and external test sets was 0.7503, 0.7512 and 0.7514, respectively. There was a significantly positive correlation between age and radscore of CN subjects (r  = 0.501; P  < .001). The radscore of MCI subjects was significantly higher than that of matched CN subjects (P  < .001). The median radscore ratios of MCI to CN from four age groups (66–70y, 71–75y, 76–80y and 81–85y) were 1.611, 1.760, 1.340 and 1.266, respectively. The probability to progression of low and high heterogeneity groups had a significant difference (P  = .002). Conclusion When radscore is significantly higher than that of normal ageing, it is necessary to alert the possibility of cognitive impairment and deterioration. [ABSTRACT FROM AUTHOR]

With the budding interests of structural and functional network characteristics as potential parameters for abnormal brains, an essential and thus simpler representation and evaluations have become necessary. Eigenvector centrality measure of functional magnetic resonance imaging (fMRI) offer region wise network representations through fMRI diagnostic maps. The article investigates the suitability of network node centrality values to discriminate ASD subject groups compared to typically developing controls following a boxplot formalism and a classification and regression tree model. Region wise differences between normal and ASD subjects primarily belong to the frontoparietal, limbic, ventral attention, default mode and visual networks. The reduced number of regions-of-interests (ROI) clearly suggests the benefit of automated supervised machine learning algorithm over the manual classification method. [ABSTRACT FROM AUTHOR]

Objective: Binge‐eating disorder is an eating disorder characterized by recurrent binge‐eating episodes, during which individuals consume excessive amounts of highly palatable food (HPF) in a short time. This study investigates the intricate relationship between repeated binge‐eating episode and the transcriptional regulation of two key genes, adenosine A2A receptor (A2AAR) and dopamine D2 receptor (D2R), in selected brain regions of rats. Method: Binge‐like eating behavior on HPF was induced through the combination of food restrictions and frustration stress (15 min exposure to HPF without access to it) in female rats, compared to control rats subjected to only restriction or only stress or none of these two conditions. After chronic binge‐eating episodes, nucleic acids were extracted from different brain regions, and gene expression levels were assessed through real‐time quantitative PCR. The methylation pattern on genes' promoters was investigated using pyrosequencing. Results: The analysis revealed A2AAR upregulation in the amygdala and in the ventral tegmental area (VTA), and D2R downregulation in the nucleus accumbens in binge‐eating rats. Concurrently, site‐specific DNA methylation alterations at gene promoters were identified in the VTA for A2AAR and in the amygdala and caudate putamen for D2R. Discussion: The alterations on A2AAR and D2R genes regulation highlight the significance of epigenetic mechanisms in the etiology of binge‐eating behavior, and underscore the potential for targeted therapeutic interventions, to prevent the development of this maladaptive feeding behavior. These findings provide valuable insights for future research in the field of eating disorders. Public Significance: Using an animal model with face, construct, and predictive validity, in which cycles of food restriction and frustration stress evoke binge‐eating behavior, we highlight the significance of epigenetic mechanisms on adenosine A2A receptor (A2AAR) and dopamine D2 receptor (D2R) genes regulation. They could represent new potential targets for the pharmacological management of eating disorders characterized by this maladaptive feeding behavior. [ABSTRACT FROM AUTHOR]

Schizophrenia and autism spectrum disorders (ASD) were considered as two neurodevelopmental disorders and had shared clinical features. we hypothesized that they have some common atypical brain functions and the purpose of this study was to explored the shared brain spontaneous activity strength alterations in early onset schizophrenia (EOS) and ASD in the children and adolescents with a multi-center large-sample study. A total of 171 EOS patients (aged 14.25 ± 1.87), 188 ASD patients (aged 9.52 ± 5.13), and 107 healthy controls (aged 11.52 ± 2.82) had scanned with Resting-fMRI and analyzed surface-based amplitude of low-frequency fluctuations (ALFF). Results showed that both EOS and ASD had hypoactivity in the primary sensorimotor regions (bilateral primary and early visual cortex, left ventral visual stream, left primary auditory cortex) and hyperactivity in the high-order transmodal regions (bilateral SFL, bilateral DLPFC, right frontal eye fields), and bilateral thalamus. EOS had more severe abnormality than ASD. This study revealed shared functional abnormalities in the primary sensorimotor regions and the high-order transmodal regions in EOS and ASD, which provided neuroimaging evidence of common changes in EOS and ASD, and may help with better early recognition and precise treatment for EOS and ASD. [ABSTRACT FROM AUTHOR]

The "brain-cognition-behavior" process is an important pathological pathway in children with attention-deficit/hyperactivity disorder (ADHD). Symptom guided multimodal neuroimaging fusion can capture behaviorally relevant and intrinsically linked structural and functional features, which can help to construct a systematic model of the pathology. Analyzing the multimodal neuroimage fusion pattern and exploring how these brain features affect executive function (EF) and leads to behavioral impairment is the focus of this study. Based on gray matter volume (GMV) and fractional amplitude of low frequency fluctuation (fALFF) for 152 ADHD and 102 healthy controls (HC), the total symptom score (TO) was set as a reference to identify co-varying components. Based on the correlation between the identified co-varying components and EF, further mediation analysis was used to explore the relationship between brain image features, EF and clinical symptoms. This study found that the abnormalities of GMV and fALFF in ADHD are mainly located in the default mode network (DMN) and prefrontal-striatal-cerebellar circuits, respectively. GMV in ADHD influences the TO through Metacognition Index, while fALFF in HC mediates the TO through behavior regulation index (BRI). Further analysis revealed that GMV in HC influences fALFF, which further modulates BRI and subsequently affects hyperactivity-impulsivity score. To conclude, structural brain abnormalities in the DMN in ADHD may affect local brain function in the prefrontal-striatal-cerebellar circuit, making it difficult to regulate EF in terms of inhibit, shift, and emotional control, and ultimately leading to hyperactive-impulsive behavior. [ABSTRACT FROM AUTHOR]

In recent years, the field of neuroimaging has undergone a paradigm shift, moving away from the traditional brain mapping approach towards the development of integrated, multivariate brain models that can predict categories of mental events. However, large interindividual differences in both brain anatomy and functional localization after standard anatomical alignment remain a major limitation in performing this type of analysis, as it leads to feature misalignment across subjects in subsequent predictive models. This article addresses this problem by developing and validating a new computational technique for reducing misalignment across individuals in functional brain systems by spatially transforming each subject's functional data to a common latent template map. Our proposed Bayesian functional group-wise registration approach allows us to assess differences in brain function across subjects and individual differences in activation topology. We achieve the probabilistic registration with inverse-consistency by utilizing the generalized Bayes framework with a loss function for the symmetric group-wise registration. It models the latent template with a Gaussian process, which helps capture spatial features in the template, producing a more precise estimation. We evaluate the method in simulation studies and apply it to data from an fMRI study of thermal pain, with the goal of using functional brain activity to predict physical pain. We find that the proposed approach allows for improved prediction of reported pain scores over conventional approaches. Received on 2 January 2017. Editorial decision on 8 June 2021 [ABSTRACT FROM AUTHOR]

Microglia sense the changes in their environment. How microglia actively translate these changes into suitable cues to adapt brain physiology is unknown. We reveal an activity-dependent regulation of cortical inhibitory synapses by microglia, driven by purinergic signaling acting on P2RX7 and mediated by microglia-derived TNFα.We demonstrate that sleep induces microgliadependent synaptic enrichment of GABAARs in a manner dependent on microglial TNFα and P2RX7. We further show that microglia-specific depletion of TNFα alters slow waves during NREM sleep and blunt memory consolidation in sleep-dependent learning tasks. Together, our results reveal that microglia orchestrate sleep-intrinsic plasticity of synaptic GABAARs, sculpt sleep slow waves, and support memory consolidation. [ABSTRACT FROM AUTHOR]

Background: Alcohol use disorder (AUD) is commonly associated with distressing psychological symptoms. Pathologic changes associated with AUD have been described in both the gut microbiome and brain, but the mechanisms underlying gut‐brain signaling in individuals with AUD are unknown. This study examined associations among the gut microbiome, brain morphometry, and clinical symptoms in treatment‐seeking individuals with AUD. Methods: We performed a secondary analysis of data collected during inpatient treatment for AUD in subjects who provided gut microbiome samples and had structural brain magnetic resonance imaging (MRI; n = 16). Shotgun metagenomics sequencing was performed, and the morphometry of brain regions of interest was calculated. Clinical symptom severity was quantified using validated instruments. Gut‐brain modules (GBMs) used to infer neuroactive signaling potential from the gut microbiome were generated in addition to microbiome features (e.g., alpha diversity and bacterial taxa abundance). Bivariate correlations were performed between MRI and clinical features, microbiome and clinical features, and MRI and microbiome features. Results: Amygdala volume was significantly associated with alpha diversity and the abundance of several bacteria including taxa classified to Blautia,Ruminococcus, Bacteroides, and Phocaeicola. There were moderate associations between amygdala volume and GBMs, including butyrate synthesis I, glutamate synthesis I, and GABA synthesis I & II, but these relationships were not significant after false discovery rate (FDR) correction. Other bacterial taxa with shared associations to MRI features and clinical symptoms included Escherichia coli and Prevotella copri. Conclusions: We identified gut microbiome features associated with MRI morphometry and AUD‐associated symptom severity. Given the small sample size and bivariate associations performed, these results require confirmation in larger samples and controls to provide meaningful clinical inferences. Nevertheless, these results will inform targeted future research on the role of the gut microbiome in gut‐brain communication and how signaling may be altered in patients with AUD. [ABSTRACT FROM AUTHOR]

Genetically encoded optical indicators and actuators of neural activity allow for all-optical investigations of signaling in the nervous system. But commonly used indicators, actuators, and expression strategies are poorly suited for systematic measurements of signal propagation at brain scale and cellular resolution. Large-scale measurements of the brain require indicators and actuators with compatible excitation spectra to avoid optical crosstalk. They must be highly expressed in every neuron but at the same time avoid lethality and permit the animal to reach adulthood. Their expression must also be compatible with additional fluorescent labels to locate and identify neurons, such as those in the NeuroPAL cell identification system. We present TWISP, a transgenic worm for interrogating signal propagation, that addresses these needs and enables optical measurements of evoked calcium activity at brain scale and cellular resolution in the nervous system of the nematode Caenorhabditis elegans. In every neuron we express a nonconventional optical actuator, the gustatory receptor homolog GUR-3 + PRDX-2 , under the control of a drug-inducible system QF + hGR, and a calcium indicator GCAMP6s, in a background with additional fluorophores from the NeuroPAL cell ID system. We show that this combination, but not others tested, avoids optical crosstalk, creates strong expression in the adult, and generates stable transgenic lines for systematic measurements of signal propagation in the worm brain. [ABSTRACT FROM AUTHOR]

Objectives Cognitive training (CT) has been investigated as a means of delaying age-related cognitive decline in older adults. However, its impact on biomarkers of age-related structural brain atrophy has rarely been investigated, leading to a gap in our understanding of the linkage between improvements in cognition and brain plasticity. This study aimed to explore the impact of CT on cognitive performance and brain structure in older adults. Methods One hundred twenty-four cognitively normal older adults recruited from 2 study sites were randomly assigned to either an adaptive CT (n  = 60) or a casual game training (active control, AC, n  = 64). Results After 10 weeks of training, CT participants showed greater improvements in the overall cognitive composite score (Cohen's d  = 0.66, p  < .01) with nonsignificant benefits after 6 months from the completion of training (Cohen's d  = 0.36, p  = .094). The CT group showed significant maintenance of the caudate volume as well as significant maintained fractional anisotropy in the left internal capsule and in left superior longitudinal fasciculus compared to the AC group. The AC group displayed an age-related decrease in these metrics of brain structure. Discussion Results from this multisite clinical trial demonstrate that the CT intervention improves cognitive performance and helps maintain caudate volume and integrity of white matter regions that are associated with cognitive control, adding to our understanding of the changes in brain structure contributing to changes in cognitive performance from adaptive CT. Clinical Trial Registration NCT03197454 [ABSTRACT FROM AUTHOR]

Rescuing memory deficits remains a major challenge in treating Alzheimer's disease (AD) and schizophrenia (SCZ). Parvalbumin interneurons (PVIs) mediate network activities relevant to memory functions. Current research suggests that the ability of PVIs to functionally adapt upon increased network activity underlies the generation of memories. The cell-type-specific interaction of neuronal plasticity on the cellular and network level (PVI cell-to-network plasticity) is a promising target in addressing memory deficits. Two clinically accessible strategies targeting PVI plasticity have emerged for the treatment of memory deficits in AD and SCZ: PVI-specific neuromodulation and high-frequency stimulation in the gamma frequency range (40 Hz). Research into clinically assessing PVI cell-to-network plasticity in humans will be essential to transfer current findings into clinical practice. Alzheimer's disease (AD) and schizophrenia (SCZ) represent two major neuropathological conditions with a high disease burden. Despite their distinct etiologies, patients suffering from AD or SCZ share a common burden of disrupted memory functions unattended by current therapies. Recent preclinical analyses highlight cell-type-specific contributions of parvalbumin interneurons (PVIs), particularly the plasticity of their cellular excitability, towards intact neuronal network function (cell-to-network plasticity) and memory performance. Here we argue that deficits of PVI cell-to-network plasticity may underlie memory deficits in AD and SCZ, and we explore two therapeutic avenues: the targeting of PVI-specific neuromodulation, including by neuropeptides, and the recruitment of network synchrony in the gamma frequency range (40 Hz) by external stimulation. We finally propose that these approaches be merged under consideration of recent insights into human brain physiology. [ABSTRACT FROM AUTHOR]

Supplemental Digital Content is Available in the Text. This is the first study in humans demonstrating noninvasive modulation of insula subregions to affect pain ratings, brain physiology related to pain (the contact heat–evoked potential), and also metrics of autonomic/cardiovascular activity including heart-rate variability. The insula is an intriguing target for pain modulation. Unfortunately, it lies deep to the cortex making spatially specific noninvasive access difficult. Here, we leverage the high spatial resolution and deep penetration depth of low-intensity focused ultrasound (LIFU) to nonsurgically modulate the anterior insula (AI) or posterior insula (PI) in humans for effect on subjective pain ratings, electroencephalographic (EEG) contact heat–evoked potentials, as well as autonomic measures including heart-rate variability (HRV). In a within-subjects, repeated-measures, pseudo-randomized trial design, 23 healthy volunteers received brief noxious heat pain stimuli to the dorsum of their right hand during continuous heart-rate, electrodermal, electrocardiography and EEG recording. Low-intensity focused ultrasound was delivered to the AI (anterior short gyrus), PI (posterior longus gyrus), or under an inert Sham condition. The primary outcome measure was pain rating. Low-intensity focused ultrasound to both AI and PI similarly reduced pain ratings but had differential effects on EEG activity. Low-intensity focused ultrasound to PI affected earlier EEG amplitudes, whereas LIFU to AI affected later EEG amplitudes. Only LIFU to the AI affected HRV as indexed by an increase in SD of N-N intervals and mean HRV low-frequency power. Taken together, LIFU is an effective noninvasive method to individually target subregions of the insula in humans for site-specific effects on brain biomarkers of pain processing and autonomic reactivity that translates to reduced perceived pain to a transient heat stimulus. [ABSTRACT FROM AUTHOR]

Objective Hydroxychloroquine (HCQ) has immunomodulatory, antithrombotic, cardiovascular, antimicrobial, and antineoplastic effects. In this study, we aimed to investigate the antiapoptotic and immunomodulator effects of intraperitoneal HCQ on hypoxic–ischemic (HI) injury in newborn rats. Study Design Wistar albino rats, 7 to 10 days old, were randomly divided into three groups: hypoxic–ischemic encephalopathy (HIE) group, HIE treated with HCQ group, and Sham group. Left common carotid artery ligation and hypoxia model were performed in HIE and HCQ groups. The HCQ group was treated with 80 mg/kg intraperitoneal HCQ every 24 hours for 3 days, while Sham and HIE groups were given physiological saline. After 72 hours, rats were decapitated and brain tissues were stained with hematoxylin and eosin, TUNEL, and IL-1β for histopathological grading and neuronal cell injury. Results Neuronal apoptosis was statistically lower in all neuroanatomical areas in the HCQ group compared with the HIE group. IL-1β-stained areas were similar in both HCQ and HIE groups but significantly higher compared with the Sham group. Histopathological grading scores were found to be lower in the HCQ group on the left parietal cortex and hippocampus region. Conclusion In this study, we have shown for the first time that HCQ treatment decreased apoptosis in HI newborn rat model in both hemispheres. HCQ may be a promising adjuvant therapy in neonatal HIE. Key Points HCQ decreased neuronal apoptosis in the ischemic penumbra of the rat brain. HCQ attenuates hypoxia–ischemia-induced brain injury in neonatal rats. HCQ has no anti-inflammatory effect on HI injury. [ABSTRACT FROM AUTHOR]

We investigated the temporal impact of multisensory settings on children's learning of word‐object and action‐object associations at 1‐ and 2‐years of age. Specifically, we examined whether the temporal alignment of words and actions influenced the acquisition of novel word‐action‐object associations. We used a preferential looking and violation of expectation task in which infants and young children were first presented with two distinct word‐object and action‐object pairings either in a synchronous (overlapping in time) or sequential manner (one after the other). Findings revealed that 2‐year‐olds recognized both, action‐object and word‐object associations when they first saw the word‐action‐object combinations synchronously, but not sequentially, as evidenced by looking behavior. 1‐year‐olds did not show evidence for recognition for either of the word‐object and action‐object pairs, regardless of the initial temporal alignment of these cues. To control for individual differences, we explored factors that might influence associative learning based on parental reports of 1‐ and 2‐year‐olds development, however, developmental measures did not explain word‐action‐object associative learning in either group. We discuss that while young children may benefit from the temporal alignment of multisensory cues as it enables them to actively engage with the multisensory content in real‐time, infants may have been overwhelmed by the complexity of this input. [ABSTRACT FROM AUTHOR]

In vitro fertilisation is a stressful process for women. Hypnofertility is a method that can be used to relieve stress during in vitro fertilisation. It is based on an effective and strong body-mind interaction, as well as balancing the brain and body via positive words and thoughts. This study aimed to investigate the effects of hypnofertility on fertility preparedness, stress, and coping with stress in women undergoing in vitro fertilisation. This study was conducted with a randomised controlled trial design. Hypnofertility-based relaxation, visualisation, imagination, and affirmation techniques were applied to the intervention group at four stages, and no initiative was applied to the women in the control group. The Clinical Trial Registration number of the study is NCT04755270. After the hypnofertility method, the mean score of the intervention group in the positive feelings and thoughts subscale of the Fertility Preparedness Scale was higher than that of the control group (p < 0.05). The hypnofertility method caused a significant decrease in the level of infertility stress in the intervention group, and the intervention group used the active-confronting and passive-avoidance methods more than control group did (p < 0.05). The hypnofertility method increased the levels of preparedness for fertility, reduced stress levels and provided effective strategies to cope with stress. [ABSTRACT FROM AUTHOR]

Patients with cancer receiving infusional chemotherapy show negative symptoms such as worry about their survival, anxiety, anguish, depression, fear, magnified perception of the passage of time, and difficulty managing boredom. Patients also suffer various side effects produced by chemotherapy such as nausea, vomiting, pain, and fatigue, which, together with psychological distress, drastically reduce their quality of life and adherence to therapy with a corresponding reduction in the probability of the individual's survival. Virtual Reality is one of the most innovative and promising digital health interventions, capable of quickly and effectively producing a positive influence on the psychosomatic axis, improving patients' quality of life during chemotherapy. Virtual Reality, through its 3-dimensional multisensory technology, isolates sensory channels from the negative external environment and enables an experience of being physically and psychologically present within virtual scenarios, in which patients can perceive sensations, emotions, cognitions, and interactions as if they really were in different surroundings. This article systematically expounds the scientific conditions necessary for effective, appropriate, and safe implementation of Virtual Reality interventions in holistic nursing practice, describing the underpinning conceptual framework, the types, technological characteristics, methods of use, duration, type of virtual content, and implementation procedure of Virtual Reality. [ABSTRACT FROM AUTHOR]

The continuing challenge of improving the quality of the biocontrol of robotic wheelchairs is addressed and a solution consisting of an integrated approach based on the combined use of gaze control and neurocontrol methods is proposed; the stages in implementing this approach are considered. The problems arising in creating gaze-controlled robotic vehicles are discussed and challenges occurring in the implementation of biocontrol and ways to solve them are analyzed. A method for selecting the most effective electroencephalography leads, based on the use of an international signal database, was developed. A convolutional neural network architecture was developed for the joint classification of eye-tracking and brain signals. Results from a study of neural networks are presented, these demonstrating a maximum prediction accuracy using the pre-trained InceptionV3 model. [ABSTRACT FROM AUTHOR]

Osteopathic manipulative treatment (OMT) is a hands-on therapy aiming to achieve the global homeostasis of the patient. OMT focuses on treating the somatic dysfunctions characterized by tissue modifications, body asymmetry, and range-of-motion restrictions. The benefits related to OMT are thought to be associated with the interconnectedness of the body's systems and the inherent capacity for self-healing. However, whether OMT can influence brain activity, and, consequently, neurophysiological responses is an open research question. Our research investigates the literature to identify the effects of OMT on brain activity. The main purpose of the research question is: can OMT influence brain activity and consequently neurophysiological responses? A scoping review was conducted, searching the following databases: PubMed, Google Scholar, and OSTEOMED.DR (Osteopathic Medical Digital Repository), Scopus, Web of Science (WoS), and Science Direct. The initial search returned 114 articles, and after removing duplicates, 69 were considered eligible to be included in the final sample. In the end, eight studies (six randomized controlled trials, one pilot study, and one cross-over study) were finally included and analyzed in this review. In conclusion, OMT seems to have a role in influencing functional changes in brain activity in healthy individuals and even more in patients with chronic musculoskeletal pain. However, further RCT studies are needed to confirm these findings. Registration protocol: CRD42024525390. [ABSTRACT FROM AUTHOR]

Background and Hypothesis This study investigated the role of the medial prefrontal cortex (mPFC)-basolateral amygdala (BLA) pathway in schizophrenia (SCZ)-related cognitive impairments using various techniques. Study Design This study utilized clinical scales, magnetic resonance imaging, single-cell RNA sequencing, and optogenetics to investigate the mPFC-BLA pathway in SCZ patients. In the mouse model, 6-week-old methylazoxymethanol acetate-induced mice demonstrated significant cognitive deficits, which were addressed through stereotaxic injections of an adeno-associated viral vector to unveil the neural connection between the mPFC and BLA. Study Results Significant disparities in brain volume and neural activity, particularly in the dorsolateral prefrontal cortex (DLPFC) and BLA regions, were found between SCZ patients and healthy controls. Additionally, we observed correlations indicating that reduced volumes of the DLPFC and BLA were associated with lower cognitive function scores. Activation of the mPFC-BLA pathway notably improved cognitive performance in the SCZ model mice, with the targeting of excitatory or inhibitory neurons alone failing to replicate this effect. Single-cell transcriptomic profiling revealed gene expression differences in excitatory and inhibitory neurons in the BLA of SCZ model mice. Notably, genes differentially expressed in the BLA of these model mice were also found in the blood exosomes of SCZ patients. Conclusions Our research provides a comprehensive understanding of the role of the PFC-BLA pathway in SCZ, underscoring its significance in cognitive impairment and offering novel diagnostic and therapeutic avenues. Additionally, our research highlights the potential of blood exosomal mRNAs as noninvasive biomarkers for SCZ diagnosis, underscoring the clinical feasibility and utility of this method. [ABSTRACT FROM AUTHOR]

Background Ventral striatal hypoactivation during reward anticipation has consistently been observed in patients with schizophrenia. In addition, that hypoactivation has been shown to correlate negatively with negative symptoms, and in particular with apathy. However, little is known about the stability of these results over time and their reliability across different centers. Methods In total, 67 patients with schizophrenia (15 females) and 55 healthy controls (13 females) were recruited in 2 centers in Switzerland and Germany. To assess the neural bases of reward anticipation, all participants performed a variant of the Monetary Incentive Delay task while undergoing event-related functional magnetic resonance imaging at baseline and after 3 months. Stability over time was measured using intra-class correlation (ICC(A,1)) and stability between centers was measured with mixed models. Results Results showed the expected ventral striatal hypoactivation in patients compared to controls during reward anticipation. We showed that these results were stable across centers. The primary analysis did not reveal an effect of time. Test-retest reliability was moderate for controls, and poor for patients. We did not find an association between ventral striatal hypoactivation and negative symptoms in patients. Conclusions Our results align with the hypothesis that ventral striatal activation is related to modulation of motivational saliency during reward anticipation. They also confirm that patients with schizophrenia show impaired reward anticipation. However, the poor test-retest reliability and the absence of an association with symptoms suggests that further research is needed before ventral striatal activity can be used as a biomarker on the individual patient level. [ABSTRACT FROM AUTHOR]

Background and Hypothesis Schizophrenia involves microstructural changes in white matter (WM) tracts. Oxidative stress is a key factor causing WM damage by hindering oligodendrocyte development and myelin maturation. Uric acid (UA), an endogenous antioxidant, may protect against oxidative stress. We investigated the effect of UA on WM connectivity in antipsychotic-naive or -free patients with early- or chronic-stage schizophrenia. Study Design A total of 192 patients with schizophrenia (122 recent-onset [ROS] and 70 chronic [CS]) and 107 healthy controls (HCs) participated in this study. Diffusion tensor imaging data and serum UA levels at baseline were obtained. Study Results Fractional anisotropy was lower in the widespread WM regions across the whole brain, and diffusivity measures were higher in both schizophrenia groups than in HCs. The CS group showed lower diffusivity in some WM tracts than the ROS or HC groups. The linear relationship of serum UA levels with axial and mean diffusivity in the right frontal region was significantly different between schizophrenia stages, which was driven by a negative association in the CS group. WM diffusivity associated with serum UA levels correlated with 8-week treatment responses only in patients with CS, suggesting UA to be protective against long-term schizophrenia. Conclusions UA may protect against the WM damage associated with the progression of schizophrenia by reducing oxidative stress and supporting WM repair against oxidative damage. These results provide insights into the positive role of UA and may facilitate the development of novel disease-modifying therapies. [ABSTRACT FROM AUTHOR]

Background and Hypothesis The brain-predicted age difference (brain-PAD) may serve as a biomarker for neurodegeneration. We investigated the brain-PAD in patients with schizophrenia (SCZ), first-episode schizophrenia spectrum disorders (FE-SSDs), and treatment-resistant schizophrenia (TRS) using structural magnetic resonance imaging (sMRI). Study Design We employed a convolutional network-based regression (SFCNR), and compared its performance with models based on three machine learning (ML) algorithms. We pretrained the SFCNR with sMRI data of 7590 healthy controls (HCs) selected from the UK Biobank. The parameters of the pretrained model were transferred to the next training phase with a new set of HCs (n  = 541). The brain-PAD was analyzed in independent HCs (n  = 209) and patients (n  = 233). Correlations between the brain-PAD and clinical measures were investigated. Study Results The SFCNR model outperformed three commonly used ML models. Advanced brain aging was observed in patients with SCZ, FE-SSDs, and TRS compared to HCs. A significant difference in brain-PAD was observed between FE-SSDs and TRS with ridge regression but not with the SFCNR model. Chlorpromazine equivalent dose and cognitive function were correlated with the brain-PAD in SCZ and FE-SSDs. Conclusions Our findings indicate that there is advanced brain aging in patients with SCZ and higher brain-PAD in SCZ can be used as a surrogate marker for cognitive dysfunction. These findings warrant further investigations on the causes of advanced brain age in SCZ. In addition, possible psychosocial and pharmacological interventions targeting brain health should be considered in early-stage SCZ patients with advanced brain age. [ABSTRACT FROM AUTHOR]

Dementia, or major neurocognitive disorder, is one of the most common causes of disability and dependency in older adults with far-reaching social, physical, and economic impacts. In the absence of adequate treatment, much research has been directed towards prevention. Physical exercise has been shown to increase cerebral blood flow, amplify production of neurotrophic factors, and enhance brain volume. Whether these changes on a structural and cellular level result in cognitive preservation is less clear. This systematic review synthesizes findings from seventeen randomized controlled trials that examine the effects of physical activity on global cognition, memory, and executive function in older adults. Cognitive benefits of exercise are strongest for those who are cognitively intact or with mild cognitive impairment. In studies with long-term follow up, cognitive gains tended to decay after cessation of physical intervention suggesting that sustained physical exercise may be required to preserve cognitive function in older adults prior to onset of dementia. [ABSTRACT FROM AUTHOR]

The molecular mechanisms underlying neuronal dysfunction in Alzheimer's disease (AD) remain uncharacterized. Here, we identify genes, molecular pathways and cellular components associated with whole-brain dysregulation caused by amyloid-beta (Aβ) and tau deposits in the living human brain. We obtained in-vivo resting-state functional MRI (rs-fMRI), Aβ- and tau-PET for 47 cognitively unimpaired and 16 AD participants from the Translational Biomarkers in Aging and Dementia cohort. Adverse neuronal activity impacts by Aβ and tau were quantified with personalized dynamical models by fitting pathology-mediated computational signals to the participant's real rs-fMRIs. Then, we detected robust brain-wide associations between the spatial profiles of Aβ-tau impacts and gene expression in the neurotypical transcriptome (Allen Human Brain Atlas). Within the obtained distinctive signature of in-vivo neuronal dysfunction, several genes have prominent roles in microglial activation and in interactions with Aβ and tau. Moreover, cellular vulnerability estimations revealed strong association of microglial expression patterns with Aβ and tau's synergistic impact on neuronal activity (q < 0.001). These results further support the central role of the immune system and neuroinflammatory pathways in AD pathogenesis. Neuronal dysregulation by AD pathologies also associated with neurotypical synaptic and developmental processes. In addition, we identified drug candidates from the vast LINCS library to halt or reduce the observed Aβ-tau effects on neuronal activity. Top-ranked pharmacological interventions target inflammatory, cancer and cardiovascular pathways, including specific medications undergoing clinical evaluation in AD. Our findings, based on the examination of molecular-pathological-functional interactions in humans, may accelerate the process of bringing effective therapies into clinical practice. [ABSTRACT FROM AUTHOR]