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This study assessed the effects of modest sleep restriction and extension on children's neurobehavioral functioning (NBF). The sleep of 77 children (age: M = 10.6 years; range = 9.1-12.2 years) was monitored for 5 nights with activity monitors. These children (39 boys and 38 girls) were all attending regular 4th- and 6th-grade classes. Their NBF was assessed using computerized tests on the 2nd day of their normal sleep schedule. On the 3rd evening, the children were asked to extend or restrict their sleep by an hour on the following 3 nights. Their NBF was reassessed on the 6th day following the experimental sleep manipulation. Sleep restriction led to improved sleep quality and to reduced reported alertness. The sleep manipulation led to significant differential effects on NBF measures. These effects may have significant developmental and clinical implications.

The aim of this study was to examine the associations between sleep and neurobehavioral functioning (NBF) in school-age children. These variables were assessed for 135 unreferred, healthy school children (69 boys and 66 girls), from second-, fourth-, and sixth-grade classes. Objective assessment methods were used on the participants in their regular home settings. Sleep was monitored using actigraphy for 5 consecutive nights; and NBF was assessed using a computerized neurobehavioral evaluation system, administered twice, at different times of the day. Significant correlations between sleep-quality measures and NBF measures were found, particularly in the younger age group. Children with fragmented sleep were characterized by lower performance on NBF measures, particularly those associated with more complex tasks such as a continuous performance test and a symbol-digit substitution test. These children also had higher rates of behavior problems as reported by their parents on the Child Behavior Checklist. These results highlight the association between sleep quality, NBF, and behavior regulation in child development; and raise important questions about the origins of these associations and their developmental and clinical significance.

Autism symptoms, including impairments in language development, social interactions, and motor skills, have been difficult to model in rodents. Since children exposed in utero to sodium valproate (VPA) demonstrate behavioral and neuroanatomical abnormalities similar to those seen in autism, the neurodevelopmental effects of this antiepileptic agent were examined in mice following its pre-or postnatal administration. Exposed pups were evaluated in a battery of neurodevelopmental procedures designed to assess VPA-induced retardation (wherein a behavior fails to mature on schedule), regression (wherein a behavior does mature on time but then deteriorates), or intrusions (wherein normal behaviors are overshadowed by stereotypic or self-injurious behaviors). The resulting observations were interpreted in the context of this new strategy to model autism.

Childhood adversity is associated with altered reward processing, but little is known about whether this varies across distinct types of adversity. In a sample of 94 children (6–19 years), we investigated whether experiences of material deprivation, emotional deprivation, and trauma have differential associations with reward‐related behavior and white matter microstructure in tracts involved in reward processing. Material deprivation (food insecurity), but not emotional deprivation or trauma, was associated with poor reward performance. Adversity‐related influences on the integrity of white matter microstructure in frontostriatal tracts varied across childhood adversity types, and reductions in frontostriatal white matter integrity mediated the association of food insecurity with depressive symptoms. These findings document distinct behavioral and neurodevelopmental consequences of specific forms of adversity that have implications for psychopathology risk.

Background Microglia‐mediated neuroinflammation plays a critical role in the pathogenesis of ischemic stroke and represents as a promising target for stroke treatment. Obacunone (OB), a triterpenoid limonin extracted from natural citrus plants, exhibits anti‐inflammatory, antioxidant and anti‐cancer properties. Method Primary microglia were pre‐incubated with OB for 2 hours, followed by LPS stimulation for 24 h or OGD treatment for 4 hours. Real‐time quantitative PCR, ELISA and western blot were performed to examine the expression levels of inflammatory cytokines. The mice were injected intraperitoneally with OB or vehicle after MCAO. Neurobehavioral tests and TTC staining were conducted to estimate the neurological deficits and infarct area. The white matter integrity after MCAO was observed via immunofluorescence staining and memroy fuctions were examined by new object recognition and MWM tests. Result We demonstrated that OB inhibit the activation of the transcription factor nuclear factor κB (NF‐κB) pathway and reduced microglia‐mediated inflammatory cytokine production both in vitro and in vivo. Furthermore, OB attenuated ischemic brain injury and cognitive impairment in mice subjected to middle cerebral artery occlusion (MCAO). Network pharmacology analysis identified mitogen‐activated protein kinase 1 gene (MAPK1/ERK2) as a potential target of OB, which was verified by the binding assays. Conclusion Our study suggest that OB alleviated neuroinflammation and ischemic injury, positioning it as a promising therapeutic agent for the treatment of ischemic stroke.

Purpose: We advanced a multifactorial, dynamic account of the complex, nonlinear interactions of motor, linguistic, and emotional factors contributing to the development of stuttering. Our purpose here is to update our account as the multifactorial dynamic pathways theory. Method: We review evidence related to how stuttering develops, including genetic/epigenetic factors; motor, linguistic, and emotional features; and advances in neuroimaging studies. We update evidence for our earlier claim: Although stuttering ultimately reflects impairment in speech sensorimotor processes, its course over the life span is strongly conditioned by linguistic and emotional factors. Results: Our current account places primary emphasis on the dynamic developmental context in which stuttering emerges and follows its course during the preschool years. Rapid changes in many neurobehavioral systems are ongoing, and critical interactions among these systems likely play a major role in determining persistence of or recovery from stuttering. Conclusion: Stuttering, or childhood onset fluency disorder (\"Diagnostic and Statistical Manual of Mental Disorders,\" 5th edition; American Psychiatric Association [APA], 2013), is a neurodevelopmental disorder that begins when neural networks supporting speech, language, and emotional functions are rapidly developing. The multifactorial dynamic pathways theory motivates experimental and clinical work to determine the specific factors that contribute to each child's pathway to the diagnosis of stuttering and those most likely to promote recovery.

Background Ischemic preconditioning (IPC) refers to the phenomenon where brief, non‐lethal episodes of ischemia protect the brain against subsequent ischemic injury. This study aims to explore the potential mechanisms underlying IPC‐induced neuroprotection in rats. Method Male and Female Wistar rats were subjected to global cerebral ischemia using the four‐vessel occlusion method. IPC was induced by subjecting animals to 5 minutes of ischemia followed by 24 hours of reperfusion before a subsequent longer ischemic insult. Behavioral, biochemical, and histological analyses were performed to evaluate the neuroprotective effects of IPC. Key parameters assessed included infarct volume, oxidative stress markers (malondialdehyde and superoxide dismutase), pro‐inflammatory cytokines (TNF‐α and IL‐6), and the expression of endogenous neuroprotective molecules such as brain‐derived neurotrophic factor (BDNF) and heat shock protein 70 (HSP70). Result Rats preconditioned with IPC showed significantly reduced infarct volume and improved neurobehavioral outcomes compared to controls. IPC significantly attenuated oxidative stress, evidenced by decreased malondialdehyde levels and increased superoxide dismutase activity. Moreover, IPC downregulated pro‐inflammatory cytokines and upregulated BDNF and HSP70 expression in the ischemic brain. These findings suggest that IPC confers neuroprotection via modulation of oxidative stress, inflammatory pathways, and induction of endogenous protective proteins. Conclusion Brain ischemic preconditioning in rats triggers multifaceted protective mechanisms, including antioxidant, anti‐inflammatory, and neurotrophic pathways. Understanding these mechanisms could provide valuable insights for developing novel therapeutic strategies to mitigate ischemic brain injury in humans. Keywords: ischemic preconditioning, neuroprotection, oxidative stress, inflammation, brain ischemia, rats

Chronic sleep deprivation has been demonstrated to diminish cognitive performance, alter mood states, and concomitantly dysregulate inflammation and stress hormones. At present, however, there is little understanding of how an acute sleep deprivation may collectively affect these factors and alter functioning. The present study aimed to determine the extent to which 24-hours of sleep deprivation influences inflammatory cytokines, stress hormones, cognitive processing across domains, and emotion states. To that end, 23 participants (mean age = 20.78 years, SD = 2.87) filled out clinical health questionnaires measured by the Pittsburgh Sleep Quality Index, Morningness Eveningness Questionnaire, and Center for Epidemiological Studies Depression Scale. Actigraph was worn for 7 days across testing to record sleep duration. At each session participants underwent a series of measures, including saliva and blood samples for quantification of leptin, ghrelin, IL-1β, IL-6, CRP, and cortisol levels, they completed a cognitive battery using an iPad, and an emotion battery. We found that an acute sleep deprivation, limited to a 24 hr period, increases negative emotion states such as anxiety, fatigue, confusion, and depression. In conjunction, sleep deprivation results in increased inflammation and decreased cortisol levels in the morning, that are accompanied by deficits in vigilance and impulsivity. Combined, these results suggest that individuals who undergo 24hr sleep deprivation will induce systemic alterations to inflammation and endocrine functioning, while concomitantly increasing negative emotions.

Increased understanding of early neurobehavioural development is needed to prevent, identify, and treat childhood psychopathology most effectively at the earliest possible stage. Prospective birth cohorts can elucidate the association of genes, environment, and their interactions with neurobehavioural development. We conducted a systematic review of the birth cohort literature. On the basis of internet searches and 6,248 peer-reviewed references, 105 longitudinal epidemiological studies were identified. Twenty studies met inclusion criteria (prospectively recruited, population-based cohort studies, including at least one assessment before the end of the perinatal period and at least one assessment of behaviour, temperament/personality, neuropsychiatric or psychiatric status before 19 years of age), and their methodologies were reviewed in full. Whilst the birth cohort studies did examine some aspects of behaviour and neurodevelopment, observations in the early months and years were rare. Furthermore, aspects of sampling method, sample size, data collection, design, and breadth and depth of measurement in some studies made research questions about neurodevelopment difficult to answer. Existing birth cohort studies have yielded limited information on how pre- and perinatal factors and early neurodevelopment relate to child psychopathology. Further epidemiological research is required with a specific focus on early neurodevelopment. Studies are needed which include the measures of early childhood psychopathology and involve long-term follow-up.

Background Alzheimer's disease (AD) is a major challenge for the global public health system. AD is the most common (60‐70%) type of dementia. Understanding the pathogenesis of AD is vital in developing effective, therapeutic or preventive strategies. The successful completion of a few late phase clinical trials and approval of monoclonal antibodies against amyloid protein in recent years reinforced the amyloid cascade hypothesis (ACH). However, the marginal efficacies of anti‐amyloid therapy and its high frequencies of side effects (e.g: ARIA‐E and AIRA‐H) indicate other major player(s) in the pathogenesis of AD and warrant more effective, safer therapies. Method In the current study, we generated recombinant Adeno‐Associated Virus (rAAV) vector expressing mouse IL‐27 (AAV‐IL‐27), enhanced green fluorescent protein (AAV‐EGFP) and Control vector (AAC‐Ctrl) without IL‐27 cDNA. AAV‐IL‐27, AAV‐EGFP or AAV‐Ctrl were delivered by stereotactic injections into the lateral ventricles of Alzheimer's disease 5xFAD mice. Mice were monitored and evaluated for various durations after a single delivery of treatment, from 4 to 7.5 months. Result Using flow cytometry and immunohistochemistry staining, we showed that intraventricular delivery of AAV‐IL‐27 successfully transduced neurons () with high levels of IL‐27 expression. Meanwhile, enhanced expression of IL‐27R were evident in regions such as the hippocampus and cerebral cortex. 5xFAD mice treated with AAV‐IL‐27 had preserved neuro‐cognitive function as revealed by neurobehavioral tests. Furthermore, AAV‐IL‐27 treatment was found to reduce the expression of pro‐inflammatory cytokine IL‐1 and limit neuronal synaptic damage. Conclusion Together with our previous reported findings, data from the current study suggest an intrinsic, neuroprotective pathway of IL‐27 that alleviates neuronal damage associated with AD via modulation of the inflammatory responses within the CNS.