Добірка наукової літератури з теми "Neurodevelopment defaults"

Default mode network (DMN) plays a central role in cognition and brain disorders. It has been shown that adverse environmental conditions impact neurodevelopment, but how these conditions impact in DMN maturation is still poorly understood. This article reviews representative neuroimaging functional studies addressing the interactions between DMN development and environmental factors, focusing on early life adversities, a critical period for brain changes. Studies focused on this period of life offer a special challenge: to disentangle the neurodevelopmental connectivity changes from those related to environmental conditions. We first summarized the literature on DMN maturation, providing an overview of both typical and atypical development patterns in childhood and early adolescence. Afterward, we focused on DMN changes associated with chronic exposure to environmental adversities during childhood. This summary suggests that changes in DMN development could be a potential allostatic neural feature associated with an embodiment of environmental circumstances. Finally, we discuss about some key methodological issues that should be considered in paradigms addressing environmental adversities and open questions for future investigations.

AbstractBackground and aimsThe clinical significance of Internet gaming disorder (IGD) is spreading worldwide, but its underlying neural mechanism still remains unclear. Moreover, the prevalence of IGD seems to be the highest in adolescents whose brains are in development. This study investigated the functional connectivity between large-scale intrinsic networks including default mode network, executive control network, and salience network. We hypothesized that adolescents with IGD would demonstrate different functional connectivity patterns among large-scale intrinsic networks, implying neurodevelopmental alterations, which might be associated with executive dysfunction.MethodsThis study included 17 male adolescents with Internet gaming disorder, and 18 age-matched male adolescents as healthy controls. Functional connectivity was examined using seed-to-voxel analysis and seed-to-seed analysis, with the nodes of large-scale intrinsic networks used as region of interests. Group independent component analysis was performed to investigate spatially independent network.ResultsWe identified aberrant functional connectivity of salience network and default mode network with the left posterior superior temporal sulcus (pSTS) in adolescents with IGD. Furthermore, functional connectivity between salience network and pSTS correlated with proneness to Internet addiction and self-reported cognitive problems. Independent component analysis revealed that pSTS was involved in social brain network.Discussion and conclusionsThe results imply that aberrant functional connectivity of social brain network with default mode network and salience network was identified in IGD that may be associated with executive dysfunction. Our results suggest that inordinate social stimuli during excessive online gaming leads to altered connections among large-scale networks during neurodevelopment of adolescents.

AbstractThe prenatal period is increasingly considered as a crucial target for the primary prevention of neurodevelopmental and psychiatric disorders. Understanding their pathophysiological mechanisms remains a great challenge. Our review reveals new insights from prenatal brain development research, involving (epi)genetic research, neuroscience, recent imaging techniques, physical modeling, and computational simulation studies. Studies examining the effect of prenatal exposure to maternal distress on offspring brain development, using brain imaging techniques, reveal effects at birth and up into adulthood. Structural and functional changes are observed in several brain regions including the prefrontal, parietal, and temporal lobes, as well as the cerebellum, hippocampus, and amygdala. Furthermore, alterations are seen in functional connectivity of amygdalar–thalamus networks and in intrinsic brain networks, including default mode and attentional networks. The observed changes underlie offspring behavioral, cognitive, emotional development, and susceptibility to neurodevelopmental and psychiatric disorders. It is concluded that used brain measures have not yet been validated with regard to sensitivity, specificity, accuracy, or robustness in predicting neurodevelopmental and psychiatric disorders. Therefore, more prospective long-term longitudinal follow-up studies starting early in pregnancy should be carried out, in order to examine brain developmental measures as mediators in mediating the link between prenatal stress and offspring behavioral, cognitive, and emotional problems and susceptibility for disorders.

Objective: This study evaluated the hypothesis that methylphenidate immediate release (MPH-IR) treatment would improve Default Mode Network (DMN) within-connectivity. Method: Resting-state functional connectivity of the main nodes of DMN was evaluated in a highly homogeneous sample of 18 drug-naive male adult participants with ADHD. Results: Comparing resting-state functional connectivity functional magnetic resonance imaging (R-fMRI) scans before and after MPH treatment focusing exclusively on within-DMN connectivity, we evidenced the strengthening of functional connectivity between two nodes of the DMN: posterior cingulate cortex (PCC) and left lateral parietal cortex (LLP). Conclusion: Our results contribute to the further understanding on how MPH affects functional connectivity within DMN of male adults with ADHD and corroborate the hypothesis of ADHD being a delayed neurodevelopmental disorder.

Objective: As two common neurodevelopmental disorders, autistic spectrum disorder and attention deficit hyperactivity disorder frequently occur together. Until now, only a few studies have investigated the co-occurrence of attention deficit hyperactivity disorder and autistic spectrum disorder, this is due to restrictions associated with previous Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. Most previous research has focused on the developmental trajectories for autistic spectrum disorder and attention deficit hyperactivity disorder separately, while the neural mechanisms underpinning the co-occurrence of autistic spectrum disorder and attention deficit hyperactivity disorder remain largely unknown. Methods: We studied 162 autistic spectrum disorder individuals (including 79 co-attention deficit hyperactivity disorder and 83 non-attention deficit hyperactivity disorder patients) and 177 typical developing individuals using resting-state functional magnetic resonance imaging data from the Autism Brain Imaging Data Exchange II, an aggregated magnetic resonance imaging dataset from 19 centers. Independent component analysis was used to extract sub-networks from the classic resting-state networks. Functional connectivity values within (intra-iFC) and between (inter-iFC) these networks were then determined. Subsequently, we compared the ASD_coADHD group with the ASD_nonADHD group in relation to the abnormal intra-iFC and inter-iFC of autistic spectrum disorder group relative to the typical developing group. Results: The ASD_coADHD group showed more severe social impairment and decreased intra-iFC in the bilateral posterior cingulate cortex of the default mode network (independent component 17) and increased inter-iFC between the default mode network (independent component 8) and the somatomotor networks (independent component 2) compared to the ASD_nonADHD group. In addition, the strength of the intra-iFC in the default mode network was associated with the severity of autistic traits across the entire autistic spectrum disorder group and particularly the ASD_coADHD group. Conclusion: Our results showed that dysfunction of the default mode network is a central feature in the co-occurrence of autistic spectrum disorder and attention deficit hyperactivity disorder, including connectivity within the default mode network as well as between the default mode network and the somatomotor networks, thus supporting the existence of a clinically combined phenotype (autistic spectrum disorder + attention deficit hyperactivity disorder).

Attention-deficit/hyperactivity disorder (ADHD) is one of the most common neurodevelopmental disorders with significant and often lifelong effects on social, emotional, and cognitive functioning. Influential neurocognitive models of ADHD link behavioral symptoms to altered connections between and within functional brain networks. Here, we investigate whether network-based theories of ADHD can be generalized to understanding variations in ADHD-related behaviors within the normal (i.e., clinically unaffected) adult population. In a large and representative sample, self-rated presence of ADHD symptoms varied widely; only 8 out of 291 participants scored in the clinical range. Subject-specific brain network graphs were modeled from functional MRI resting-state data and revealed significant associations between (nonclinical) ADHD symptoms and region-specific profiles of between-module and within-module connectivity. Effects were located in brain regions associated with multiple neuronal systems including the default-mode network, the salience network, and the central executive system. Our results are consistent with network perspectives of ADHD and provide further evidence for the relevance of an appropriate information transfer between task-negative (default-mode) and task-positive brain regions. More generally, our findings support a dimensional conceptualization of ADHD and contribute to a growing understanding of cognition as an emerging property of functional brain networks.

Congenital amusia, a neurodevelopmental disorder of music perception and production, has been associated with abnormal anatomical and functional connectivity in a right frontotemporal pathway. To investigate whether spontaneous connectivity in brain networks involving the auditory cortex is altered in the amusic brain, we ran a seed-based connectivity analysis, contrasting at-rest functional MRI data of amusic and matched control participants. Our results reveal reduced frontotemporal connectivity in amusia during resting state, as well as an overconnectivity between the auditory cortex and the default mode network (DMN). The findings suggest that the auditory cortex is intrinsically more engaged toward internal processes and less available to external stimuli in amusics compared with controls. Beyond amusia, our findings provide new evidence for the link between cognitive deficits in pathology and abnormalities in the connectivity between sensory areas and the DMN at rest.

IntroductionAttention deficit hyperactivity disorder (ADHD) is a challenge in child and adolescent psychiatry. In the recent decades many studies with longitudinal designs have used neuroimaging with ADHD patients, suggesting its neurodevelopmental origin.ObjectivesStudy the findings of neuroimaging (MRI, fMRI, DTI, PET) techniques on ADHD patients from a longitudinal point of view, looking also for the potential influence of treatments and other predictors (i.e. genetics).AimsTo provide a global perspective of all the recent findings on ADHD patients with the neuroimaging technics, focusing on longitudinal measurements of the changes in brain development.MethodsWe conducted a review of the literature in the databases Pubmed and ScienceDirect (terms ADHD, neuroimaging, MRI, fMRI, DTI, PET, functional connectivity, metilphenidate and cortical thickness). We focused on studies using neuroimaging techniques with ADHD patients, looking at their populations, methodologies and results.ResultsThe studies found abnormalities in the structure of grey matter, activity and brain connectivity in many neural networks, with particular involvement of the fronto-parietal and Default Mode Network. There is also convergent evidence for white matter pathology and disrupted anatomical connectivity in ADHD. In addition, dysfunctional connectivity during rest and during cognitive tasks has been demonstrated.ConclusionsThis evidence describe ADHD as a brain development disorder, with delays and disruptions in the global development of the central nervous system that compromises grey and white matters, most evident in the prefrontal cortex, parietal and posterior cingulate cortices, as well as basal ganglia, damaging activity and structural and functional connectivity of various brain networks, especially the fronto-striato-parietal and default mode network.Disclosure of interestThe authors have not supplied their declaration of competing interest.

IntroductionADHD is a neurodevelopmental disorder comprising brain structural and functional alterations, especially in default mode network (DMN), as MRI studies have recently shown. However, it is not clear in which extent medication for ADHD may influence the activity of these networks.ObjectivesThe main purpose is to look up published evidence about the effects of ADHD medication on the connectivity of DMN in patients as measured with functional-MRI.MethodsA review was conducted with Pubmed, using search terms ‘default mode network’+ ‘ADHD’ + ‘medication’/‘methylphenidate’/‘atomoxetine’/‘stimulant’/‘lisdexanfetamine’. Original research studies in English using f-MRI to assess DMN connectivity in ADHD patients were included in a more comprehensive review.ResultsThe searches found 124 articles, 8 meeting the review criteria. A total size of 146 ADHD patients was comprised (mean size: 18.25 patients). Three studies used specific resting-state f-MRI. Seven were drug trials, 3 of them short-term, randomized and controlled ones. Six included methylphenidate, 2 atomoxetine, 1 lisdexanfetamine and 3 amphetamines. Two also assessed drugs clinical effects. Evidence seems heterogeneous, but mostly consistent with normalizing drug effects on DMN in patients (in some studies also compared with healthy controls), associated with a measured clinical improvement in one study with amphetamines and one with atomoxetine. One trial found little differences on DMN activity.ConclusionsPsychostimulant drugs and atomoxetine are clinically effective medications; DMN connectivity may partially explain their action mechanisms and constitute a potential response predictor. Further f-MRI studies might more deeply assess the imaging-clinical relationships for each drug.Disclosure of interestThe authors have not supplied their declaration of competing interest.

L'épilepsie est une maladie neurologique qui touche plus de 50 millions de personnes dans le monde. Elle se caractérise par des crises récurrentes dues à la surexcitation synchrone et spontanée de populations neuronales du cerveau. Les crises sont de nature très variable et les symptômes dépendent de la zone du cerveau touchée et de son étendue. Le terme «troubles épileptiques» est par conséquent préféré. Ceux-ci peuvent avoir de nombreuses causes, soient génétiques (par exemple, le syndrome de Dravet, une épilepsie infantile rare, provoquée dans 80% des cas par la mutation hétérozygote du gène SCN1A), soient environnementales (par exemple, après un empoisonnement aux organophosphorés, des composés présents dans les pesticides et les agents de guerre neurotoxiques). Dans les deux cas, les traitements actuels ne permettent pas un contrôle optimal des crises. Une meilleure compréhension de la physiopathologie de ces différentes formes d'épilepsie est donc nécessaire pour trouver de nouvelles cibles thérapeutiques et de nouveaux anticonvulsivants. Les cellules microgliales, les macrophages résidents du cerveau ont de nombreuses fonctions qui varient en fonction de la maturité du cerveau. Les microglies sont les gardiennes de l'homéostasie cérébrale, assurant en permanence le bon fonctionnement des neurones. Ce sont des cellules immunitaires capables de moduler leur activité en fonction des dangers qu'elles détectent. De plus, elles ont un rôle particulier dans la plasticité synaptique et la modulation de l'excitabilité neuronale. Ces différents rôles ont suscité de nombreuses hypothèses sur l'implication de ces cellules dans la physiopathologie des troubles épileptiques. Pour certaines, les microglies sont nocives pour l'excitabilité des neurones, par leur activation et la sécrétion chronique de cytokines pro-inflammatoires. Pour d'autres, elles ont un rôle bénéfique, la microglie tamponnant l'hyperexcitabilité neuronale et diminuant ainsi la fréquence des crises. L'objectif de mon travail de thèse était d'étudier les mécanismes de l'épileptogenèse impliquant les cellules microgliales afin d'identifier de nouvelles cibles thérapeutiques. J'ai développé deux modèles d'épilepsie chez le poisson zèbre, un modèle génétique du syndrome de Dravet et un modèle d'empoisonnement aux organophosphorés. Ceux-ci m'ont permis d'étudier les modifications du système nerveux central au cours de l'épileptogenèse. J'ai ainsi montré un déséquilibre de la balance excitateur/inhibiteur vers l'excitation qui pourrait déclencher des crises d'épilepsie. En utilisant le modèle de Dravet, j'ai également caractérisé les changements morphologiques, comportementaux et moléculaires des cellules microgliales après des crises. Ces travaux améliorent notre compréhension des conséquences des crises d'épilepsie dans le cerveau et contribuent à ouvrir la voie à la découverte de nouvelles cibles thérapeutiques pour traiter différentes formes d'épilepsie
Epilepsy is a neurological disease affecting some 50 million people worldwide. It is characterized by recurrent seizures due to the synchronous and spontaneous overexcitation of neuronal populations in the brain. Seizures vary widely in nature, and symptoms dependon the area of the brain affected and its extent. The term ‘epileptic disorders’ is accordingly preferred. These can have many causes, including both genetic (e.g. Dravet syndrome, a rare infantile epilepsy caused in 80% of cases by the heterozygous mutation of the SCN1A gene), and environmental (e.g. after poisoning with organophosphates, compounds present in pesticides and neurotoxic warfare agents). Whether for Dravet syndrome or organophosphate poisoning, current treatments do not enable optimal control of seizures. A better understanding of the pathophysiology of these different forms of epilepsy is thus needed to find new therapeutic targets and new anticonvulsants. Microglial cells are the resident macrophages in the brain. These cells have many functions, which can vary depending on the maturity of the brain. The microglia are the guardians of cerebral homeostasis, continuously ensuring the proper functioning of neurons. They are immune cells able to modulate their activity according to the dangers they detect. In addition, microglia have a special role in synaptic plasticity and the modulation of neuronal excitability. These different roles have prompted numerous hypotheses on the involvement of these cells in the pathophysiology of epileptic disorders. In some, microglia are harmful for the excitability of neurons, through their activation and the chronic secretion of proinflammatory cytokines. Others lend them a beneficial role, with microglia buffering neuronal hyperexcitability and thus decreasing the frequency of seizures. The objective of my PhD work was to study the mechanisms of epileptogenesis involving microglial cells in order to identify new therapeutic targets. I developed two models of epilepsy in zebrafish, a genetic model of Dravet syndrome and a model of organophosphate poisoning. These enabled me to study the modifications of the central nervous system during epileptogenesis. I specifically demonstrated an excitatory/inhibitory imbalance toward excitation that could trigger epileptic seizures. Using the Dravet model, I also successfully characterized the morphological, behavioral and molecular changes of microglial cells after seizures. This work improves our understanding of the consequences of epileptic seizures in the brain and helps pave the way for the discovery of new therapeutic targets to treat different forms of epilepsy

This chapter addresses functional magnetic resonance imaging (fMRI) of brain in children with neurodevelopmental and behavioral disorders. Common challenges of pediatric fMRI studies are related to acquisition and processing. In children with disruptive behavior disorders, deficits in affective response, empathy, and decision-making have been reported. Resting-state fMRI studies in attention-deficit hyperactivity disorder (ADHD) have shown altered activity in default mode and cognitive control networks. Task-based fMRI studies in ADHD have implicated frontoparietal cognitive and attentional networks. The role of stimulants in restoring the altered brain function has been examined using fMRI studies. In children with autism spectrum disorder, fMRI studies using face-processing tasks, theory-of-mind tasks, imitation, and language processing (e.g., sentence comprehension), as well as studies of gaze aversion, interest in social faces, and faces with emotions have implicated cerebellum, amygdala, hippocampus, insula, fusiform gyrus, superior temporal sulcus, planum temporale, inferior frontal gyrus, basal ganglia, thalamus, cingulate cortex, corpus callosum, and brainstem. In addition, fMRI has been a valuable research tool for understanding neurobiological substrates in children with psychiatric disorders (e.g., psychosis, posttraumatic stress disorder, and anxiety disorders).

Psychotic disorders such as schizophrenia are serious, common, and highly disabling illnesses. Their pathophysiologies remain unclear, and have been a subject of many theories. In recent years, there has been considerable progress in understanding the pathophysiology of the early course of psychoses, as it pertains to the adolescent onset of these illnesses. This chapter summarizes recent literature and the authors’ work in the neurobiology of early-course psychotic disorders using neurocognitive, structural, functional, and spectroscopic neuroimaging, as well as electrophysiological and sleep studies. Extant literature and the authors’ studies suggest alterations in cognition, brain structure, function, and neurochemistry in the early course of psychotic illnesses and in young relatives at risk for this illness. The literature points to alterations in grey matter volumes and white matter connectivity across several key brain regions, aberrations in task and default network function. Spectroscopy and PET studies suggest alterations in glutamatergic and dopaminergic neurotransmission. These alterations begin around early adolescence and progress during the early phases of psychotic illnesses. Pathophysiology might be related to a neurodevelopmental derailment involving aberrations in programmed synaptic refinement and plasticity processes. Recent genetic data point to the involvement of developmental, immune, glutamatergic, and dopaminergic function. These emerging insights may suggest novel targets for prevention and early intervention.