Brain development

This review considers the research to date on the role of nutrition in cognitive development in children, with a particular emphasis on the relatively neglected post-infancy period. Undernutrition and deficiencies of iodine, iron, and folate are all important for the development of the brain and the emergent cognitive functions, and there is some evidence to suggest that zinc, vitamin B 12 , and omega-3 polyunsaturated fatty acids may also be important. Considerations for future research include a focus on the interactions between micronutrients and macronutrients that might be influential in the optimization of cognitive development; investigation of the impact of nutritional factors in children after infancy, with particular emphasis on effects on the developing executive functions; and selection of populations that might benefit from nutritional interventions, for example, children with nutrient deficiencies or those suffering from attention deficit-hyperactivity disorder and dyslexia.

This article reviews recent findings in the developmental neurophysiology of children subjected to psychological trauma. Studies link extreme neglect and abuse with long-term changes in the nervous and endocrine systems. A growing body of research literature indicates that individuals with severe trauma histories are at higher risk of behaving violently than those without such histories. This article links these two research areas by discussing how severe and protracted child abuse and/or neglect can lead to biological changes, putting these individuals at greater risk for committing homicide and other forms of violence than those without child maltreatment histories. The implications of these biological findings for forensic evaluations are discussed. Based on new understanding of the effects of child maltreatment, the authors invite law and mental health professionals to rethink their notions of justice and offender accountability, and they challenge policymakers to allocate funds for research into effective treatment and for service delivery.

Prenatal stress (PS) has been linked to abnormal cognitive, behavioral and psychosocial outcomes in both animals and humans. Animal studies have clearly demonstrated PS effects on the offspring's brain, however, while it has been speculated that PS most likely affects the brains of exposed human fetuses as well, no study has to date examined this possibility prospectively using an independent stressor (i.e., a stressful event that the pregnant woman has no control over, such as a natural disaster). The aim of this review is to summarize the existing animal literature by focusing on specific brain regions that have been shown to be affected by PS both macroscopically and microscopically. These regions include the hippocampus, amygdala, corpus callosum, anterior commissure, cerebral cortex, cerebellum and hypothalamus. We first discuss the mechanisms by which the effects of PS might occur. In particular, we show that maternal and fetal hypothalamicpituitary-adrenal (HPA) axes, and the placenta, are the most likely candidates for these mechanisms. We see that, although animal studies have obvious advantages over human studies, the integration of findings in animals and the transfer of these findings to human populations remains a complex issue. Finally, we show how it is possible to circumvent these challenges by studying the effects of PS on brain development directly in humans, by taking advantage of natural or man-made disasters and assessing the impact and consequences of such stressful events on pregnant women and their offspring prospectively. cortex; SDN-MPOA, sexually dimorphic nucleus of the medial preoptic area; AVPV, anteroventral periventricular nucleus 0165-0173/$see front matter

Over the last ten years the basic knowledge of brain structure and function has vastly expanded, and its incorporation into the developmental sciences is now allowing for more complex and heuristic models of human infancy. In a continuation of this effort, in this two-part work I integrate current interdisciplinary data from attachment studies on dyadic affective communications, neuroscience on the early developing right brain, psychophysiology on stress systems, and psychiatry on psychopathogenesis to provide a deeper understanding of the psychoneurobiological mechanisms that underlie infant mental health. In this article I detail the neurobiology of a secure attachment, an exemplar of adaptive infant mental health, and focus upon the primary caregiver's psychobiological regulation of the infant's maturing limbic system, the brain areas specialized for adapting to a rapidly changing environment. The infant's early developing right hemisphere has deep connections into the limbic and autonomic nervous systems and is dominant for the human stress response, and in this manner the attachment relationship facilitates the expansion of the child's coping capcities. This model suggests that adaptive infant mental health can be fundamentally defined as the earliest expression of flexible strategies for coping with the novelty and stress that is inherent in human interactions. This efficient right brain function is a resilience factor for optimal development over the later stages of the life cycle.

Studies over the last decade demonstrate that adolescence is a brain maturation period from childhood to adulthood. Plastic and dynamic processes drive adolescent brain development, creating flexibility that allows the brain to refine itself, specialize, and sharpen its functions for specific demands. Maturing connections enable increased communication among brain regions, allowing greater integration and complexity. Compelling evidence has shown that the developing brain is vulnerable to the damaging effects of ethanol. It is possible to infer, therefore, that alcohol exposure during the critical adolescent developmental stages could disrupt the brain plasticity and maturation processes, resulting in behavioral and cognitive deficits. Recent neuroimaging studies have provided evidence of the impact of human adolescent drinking in brain structure and functions. Findings in experimental animals have also given new insight into the potential mechanisms of the toxic effects of ethanol on both adolescent brain maturation and the short-and long-term cognitive consequences of adolescent drinking.

Recent studies have focused on the behavioral and neurobiological sequella of exposure to early adverse events. We hypothesize that early adverse experiences result in an increased sensitivity to the effects of stress later in life and render an individual vulnerable to stress-related psychiatric disorders. This vulnerability may be mediated by persistent changes in corticotropin-releasing-factor (CRF)-containing neurons, the hypothalamic-pituitary-adrenal axis, and the sympathetic nervous system. We therefore present an overview of the CRF system and its role as a mediator in the development of the stress response, major depression, and posttraumatic stress disorder. The literature pertaining to behavioral and neurobiological alterations associated with exposure to early adverse life events in rodents, nonhuman primates, and humans is reviewed. We focus on animal models that precipitate depressive and anxiety symptoms while producing neuroendocrine alterations that mimic those seen in adults with those disorders. The literature integrating neurobiological and behavioral consequences of early life stress is also reviewed, focusing primarily on infants born to mothers with depression and on infants who were abused or neglected.

Both epidemiologic data and everyday life experience show that adolescents adopt risktaking behaviours, that increase the morbidity and mortality rates, despite a general body strengthening. This phenomenon could suggest the presence of a still immature capacity of judgement and evaluation of consequences of one own actions. Recent evidence, from neuroscience, gives a possible explanation for this kind of adolescent behaviour. New studies on neuroeconomics describe the prefrontal cortex as one of the most important centres of the neural circuits involved in decision-making. Longitudinal studies with structural neuroimaging techniques show that the prefrontal cortex undergoes important changes during adolescence, in terms of synapse number and myelination. If affective executive functions, especially decision-making processes, are based on prefrontal cortex areas that mature during adolescence, it is possible to deem that adolescent decision-making is still a work in progress, and this could contribute to better explain their risk-taking behaviours. These data then have to be related with the several psychopathological disorders with an adolescence onset.

Autism is a neurodevelopmental disorder that severely disrupts social and cognitive functions. MRI is the method of choice for in vivo and non-invasively investigating human brain morphology in children and adolescents. The authors reviewed structural MRI studies that investigated structural brain anatomy and development in autistic patients. All original MRI research papers involving autistic patients, published from 1966 to May 2003, were reviewed in order to elucidate brain anatomy and development of autism and rated for completeness using a 12-item check-list. Increased total brain, parieto-temporal lobe, and cerebellar hemisphere volumes were the most replicated abnormalities in autism. Interestingly, recent findings suggested that the size of amygdala, hippocampus, and corpus callosum may also be abnormal. It is conceivable that abnormalities in neural network involving fronto-temporo-parietal cortex, limbic system, and cerebellum may underlie the pathophysiology of autism, and that such changes could result from abnormal brain development during early life. Nonetheless, available MRI studies were often conflicting and could have been limited by methodological issues. Future MRI investigations should include well-characterized groups of autistic and matched healthy individuals, while taking into consideration confounding factors such as IQ, and socioeconomic status.

Developmental and social factors are known to play a crucial role in the pathogenesis of affective disorders. Although it has been demonstrated that early life aversive experiences can be a risk factor in the development of human depression, most of the investigation in animals that try to model depression do not include postnatal manipulations. Since housing represents a fundamental ethological factor which modifies behavior and brain development, this study aimed to investigate the impact of different social and structural housing conditions on the development of a depressive-like syndrome in the behavioral despair paradigm and an anxiety-like syndrome in the unconditioned anxiety paradigm. The present study uses several multivariate analyses to study the impact of housing conditions in animal models of depression and anxiety. In this study, social isolation was able to reproduce the effects found in other animals models based on stress, suggesting that only 2 months of social isolation are enough to produce effects that can be useful as behavioral model of depression. Moreover, environmental enrichment showed an antidepressive and anxiolytic like effect in animal models of depression and anxiety. This effect, which has not been reported in earlier studies, suggests that stimulation during the first stages of growth might play a "protective" role on behavior and brain development.

Otizmin de içinde bulundu¤u yayg›n geliflimsel bozukluklar (YGB) iletiflim, sosyal bilifl ve duygusal iflaretlerin ifllenmesi gibi kifliler aras› iliflkileri oluflturan birçok alanda ciddi ve süregen bozukluklarla karakterize, genetik temelleri olan ve anormal beyin gelifliminin görüldü¤ü nörogeliflimsel hastal›klard›r. Otistik bozukluk (OB) ve di¤er YGB'si olan çocuklardaki biliflsel yetersizlikler; zihin kuram› bozuklu¤u, yürütücü ifllev bozuklu-¤u ve zay›f merkezi bütünleflme gibi nöropsikiyatrik modellerle aç›klanmaya çal›fl›lmaktad›r. Bu makalede YGB'de sosyal bilifli aç›klamaya çal›flan zihin kuram› ve sosyal biliflin nörobiyolojik temellerinin gözden geçirilmesi amaçlanm›flt›r. OB ve di¤er YGB'deki sosyal bilifl ve zihin kuram›n› inceleyen ça-l›flmalara PubMed arama motoru kullan›larak ulafl›lm›fl ve elde edilen veriler bu derleme kapsam›nda ele al›nm›flt›r. Sosyal bilifl, di¤erlerinin düflüncelerini ve niyetlerini anlayabilme arac›l›¤›yla onlar›n davran›fllar›n›n anlam›n› ç›karabilme, öngörebilme ve karmafl›k sosyal çevreler ile etkileflime girebilme yetene¤i olarak tan›mlanabilir. Zihin kuram› yetersizli¤i OB'deki temel sorunlardan biridir ve otizmi olan bireylerde zihinsel süreçlerin kavranmas›nda, kendi zihinsel temsillerinin ve di¤er in-sanlar›n zihinsel temsillerinin kavranmas›nda yetersizlik bulun-maktad›r. OB olan bireylerde, normalde olmas› gereken, yüz ta-n›ma, göz göze iliflki kurma, yüzdeki emosyonu okuma gibi, ki-flileraras› iliflkilerin ve sosyal gruptaki ifllevselli¤in önemli bir parças› olan sosyal ifllevlerin bozuklu¤u söz konusudur. Sosyal bilifl ile iliflkili beyin alanlar›; frontal lob, temporal lob, ön singulat korteks, fusiform girus, amigdala, ve arka assosiasyon korteksi ile bunlar›n iç ba¤lant›lar›d›r. Fusiform girus ve amigdala yüz tan›ma ve alg›lamas›nda görev al›r ve yap›lan çal›flmalarda özellikle erken geliflim dönemlerinde amigdaladaki bir bozuklu¤un, ileride yüz kimli¤i ve yüz ifadelerinin d›flavurumunu alg›lamada sosyal alg›sal bozukluklara yol açt›¤›ndan bahsedilmektedir. YGB'si olan bireylerin yüzleri alg›larken fusiform girus aktivasyonunda düflüklük saptanm›flt›r. Amigdalan›n fusiform girus üzerine düzenleyici bir etkisi bulundu¤undan, amigdala lezyonlar›nda, emosyon yüklü yüzlere karfl› fusiform girusdaki azalm›fl aktivasyon, amigdaladaki ifllevsizli¤in derecesiyle ba¤lant›l›d›r. Birçok çal›flman›n ortak bulgusu, OB'deki fusiform girus hipoaktivasyonunun amigdalaya ba¤l› baz› süreçlerden kaynakland›¤› yönündedir. OB olan bireylerde, gözlerin bak›fl yönü, hareketleri ve karfl›daki kiflinin beden hareketlerinden sosyal uyaran›n anlafl›lmas›nda rolü bulunan üst temporal sulkusun hipoaktivasyonu ve anormal hacim ölçümleri saptanm›fl-t›r. Temelde bir sosyal bilifl bozuklu¤u oldu¤unu söyleyebilece-¤imiz OB, beynin bu sistemlerinin mikroskopik ve/veya makroskopik düzeydeki aksakl›klar›na ba¤l› olarak a盤a ç›kmaktad›r. Sonuç olarak, OB ve di¤er YGB'de sosyal bilifl nörobiyolojisine bak›ld›¤›nda, erken bebeklikte amigdalada ve amigdalan›n fusiform girus, üst temporal sulkusu içeren di¤er temporal alanlarla ba¤lant›s›nda varolan bir bozuklu¤un, çocu¤un yüzlere ve di¤er sosyal olarak anlaml› olan uyaranlara karfl› ilgisinin azal-mas›na ya da yok olmas›na neden oldu¤u görülmektedir. Bu da normal uyarana ba¤l› aktivasyon gerektiren fusiform girus gibi beyin bölgelerinin normal geliflimlerinden sapmas›na neden oldu¤u anlafl›lmaktad›r. Otizmdeki sosyal kognisyon sorunlar›n›n anlafl›lmas› üzerine çal›-fl›rken, temelde bilinmesi gereken fley, otizmin bir tek nöroanatomik yap› ya da döngünün hastal›¤› de¤il, daha yayg›n, birçok nöronal sistemin etkilendi¤i nörogeliflimsel bir bozukluk oldu¤udur. Anahtar sözcükler: Otizm, yayg›n geliflimsel bozukluklar, zihin kuram›, sosyal bilifl Klinik Psikofarmakoloji Bülteni 2009;19:322-331 ABSTRACT:

Neuropsychological research has permitted defining specific cognitive profiles among individuals with mental retardation (MR) of different etiology. Namely, the cognitive profile of people with Down syndrome (DS) is often reported to be characterized by a deficit in language abilities that usually exceed impairments in visual-spatial capacities. However, recent studies have demonstrated a more complex neuropsychological profile in this population, with atypical development in the cognitive and in the linguistic domain. This paper is dedicated to reviewing literature regarding motor, linguistic and cognitive abilities in DS. Our aim is to present evidences supporting the hypothesis that individuals with these syndrome exhibit a peculiar motor development and neuropsychological profile with some abilities more preserved and others more impaired. This finding may have theoretical and practical implications. In fact, a better definition of the cognitive pattern in DS may contribute to understand the nature of MR in general and, also, it may suggests individualized rehabilitation treatment protocols.

Neural Darwinism (ND) is a large scale selectionist theory of brain development and function that has been hypothesized to relate to consciousness. According to ND, consciousness is entailed by reentrant interactions among neuronal populations in the thalamocortical system (the Ôdynamic coreÕ). These interactions, which permit high-order discriminations among possible core states, confer selective advantages on organisms possessing them by linking current perceptual events to a past history of value-dependent learning. Here, we assess the consistency of ND with 16 widely recognized properties of consciousness, both physiological (for example, consciousness is associated with widespread, relatively fast, low amplitude interactions in the thalamocortical system), and phenomenal (for example, consciousness involves the existence of a private flow of events available only to the experiencing subject). While no theory accounts fully for all of these properties at present, we find that ND and its recent extensions fare well.

Recent structural and functional imaging studies have provided evidence for continued development of brain regions involved in social cognition during adolescence. In this paper, we review this rapidly expanding area of neuroscience and describe models of neurocognitive development that have emerged recently. One implication of these models is that neural development underlies commonly observed adolescent phenomena such as susceptibility to peer influence and sensitivity to peer rejection. Experimental behavioural evidence of rejection sensitivity in adolescence is currently sparse. Here, we describe a study that directly compared the affective consequences of an experimental ostracism manipulation (Cyberball) in female adolescents and adults. The ostracism condition led to significantly greater affective consequences in the adolescents compared with adults. This suggests that the ability to regulate distress resulting from ostracism continues to develop between adolescence and adulthood. The results are discussed in the context of models of neurocognitive development.

Educational neuroscience is an emerging effort to integrate neuroscience methods, particularly functional neuroimaging, with behavioral methods to address issues of learning and instruction. This article consolidates common concerns about connecting education and neuroscience. One set of concerns is scientific: in-principle differences in methods, data, theory, and philosophy. The other set of concerns is pragmatic: considerations of costs, timing, locus of control, and likely payoffs. The authors first articulate the concerns and then revisit them, reinterpreting them as potential opportunities. They also provide instances of neuroscience findings and methods that are relevant to education. The goal is to offer education researchers a window into contemporary neuroscience to prepare them to think more specifically about the prospects of educational neuroscience.

During the last few decades our understanding of the possible role of thyroid hormones during brain development has increased and contributed to resolve previously discordant hypotheses, although much remains to be clarified. Thyroid hormones of maternal origin are present in the fetal compartment, despite the very efficient uterine-placental 'barrier', necessary to avoid potentially toxic concentrations of free T4 and T3 from reaching fetal tissues before they are required for development. T3 remains low throughout pregnancy, whereas FT4 in fetal fluids increases rapidly to adult levels, and is determined by the maternal availability of T4. It is present in embryonic fluids 4 weeks after conception, with FT4 steadily increasing to biologically relevant values. T3, generated from T4 in the cerebral cortex, reaches adult values by mid-gestation and is partly bound to specific nuclear receptor isoforms. Iodothyronine deioidinases are important for the spatial and temporal regulation of T3 bioavailability, tailored to the differing and changing requirements of thyroid hormone-sensitive genes in different brain structures, but other regulatory mechanism(s) are likely to be involved. Maternal transfer constitutes a major fraction of fetal serum T4, even after onset of fetal thyroid secretion, and continues to have an important protective role in fetal neurodevelopment until birth.

Caspases are crucial mediators of programmed cell death (apoptosis). Among them, caspase-3 is a frequently activated death protease, catalyzing the specific cleavage of many key cellular proteins. However, the specific requirements of this (or any other) caspase in apoptosis have remained largely unknown until now. Pathways to caspase-3 activation have been identified that are either dependent on or independent of mitochondrial cytochrome c release and caspase-9 function. Caspase-3 is essential for normal brain development and is important or essential in other apoptotic scenarios in a remarkable tissue-, cell type-or death stimulus-specific manner. Caspase-3 is also required for some typical hallmarks of apoptosis, and is indispensable for apoptotic chromatin condensation and DNA fragmentation in all cell types examined. Thus, caspase-3 is essential for certain processes associated with the dismantling of the cell and the formation of apoptotic bodies, but it may also function before or at the stage when commitment to loss of cell viability is made.

We describe an integrated theory of individual diVerences that traces the behavioral development of life history from genes to brain to reproductive strategy. We provide evidence that a single common factor, the K-Factor, underpins a variety of life-history parameters, including an assortment of sexual, reproductive, parental, familial, and social behaviors. We explore the psychometrics and behavioral genetics of the K-Factor and oVer a speculative account of the proximate mediation of this adaptive patterning of behavior as instantiated in well-established functions of speciWc areas of the human brain, including the frontal lobes, amygdala, and hippocampus. We then apply Life History Theory to predict patterns of development within the brain that are paedomorphic (i.e., development begins later, proceeds at a slower rate, and has an earlier cessation) and peramorphic (i.e., development begins early, proceeds at a faster rate, and has a later cessation).

The ω-3 fatty acids are essential dietary nutrients and one of their important roles is providing the fatty acid with 22 carbons and 6 double bonds known as docosahexaenoic acid (DHA) for nervous tissue growth and function. Inadequate intakes of ω-3 fatty acids decrease DHA and increase ω-6 fatty acids in the brain. Decreased DHA in the developing brain leads to deficits in neurogenesis, neurotransmitter metabolism, and altered learning and visual function in animals. Western diets are low in ω-3 fatty acids, including the 18 carbon ω-3 fatty acid alpha linolenic acid found mainly in plant oils, and DHA, which is found mainly in fish. The DHA status of the newborn and breast-fed infant depends on the maternal intake of DHA and varies widely. Epidemiological studies have linked low maternal DHA to increased risk of poor child neural development. Intervention studies have shown improving maternal DHA nutrition decreases the risk of poor infant and child visual and neural development. Thus, sufficient evidence is available to conclude that maternal fatty acid nutrition is important to DHA transfer to the infant before and after birth, with short and long-term implications for neural function. However, genetic variation in genes encoding fatty acid desaturases also influence essential fatty acid metabolism, and may increase requirements in some individuals. Consideration of ω-3 fatty acid to include brain development, optimizing ω-3 and ω-6 fatty acids in gestation and lactation, and in fatty acid nutrition support for intravenous and formula-fed neonates is important.

Autism is one of the most heritable neurodevelopmental conditions and has an early onset, with symptoms being required to be present in the first 3 years of life in order to meet criteria for the 'core' disorder in the classification systems. As such, the focus on identifying a prodrome over the past 20 years has been on pre-clinical signs or indicators that will be present very early in life, certainly in infancy. A number of novel lines of investigation have been used to this end, including retrospective coding of home videos, prospective population screening and 'high risk' sibling studies; as well as the investigation of pre-and peri-natal, brain developmental and other biological factors. While no single prodromal sign is expected to be present in all cases, a picture is emerging of indicative prodromal signs in infancy and initial studies are being undertaken to attempt to ameliorate early presentation and even 'prevent' emergence of the full syndrome.

The primary aim of this paper is to explore some of the issues surrounding the concept of DCD as a``speci®c'' learning diculty. Questions relating to the assessment and identi®cation of DCD are addressed. The arguments we present are derived from data obtained in a study which compared 224 children referred because of learning and attention problems (but not motor diculties) and 155 typically developing children. These 379 children were all assessed on a range of formal and informal tests, including several sensorimotor tests. Working criteria for classifying a child as DCD were derived. In addition to the high prevalence ®gures obtained for DCD in this group of children, the degree of comorbidity observed between DCD and the other developmental disorders (reading disability and attention-de®cit/hyperactivity disorder) was also striking. These results prompted us to re-evaluate the usefulness of discrete diagnostic categories, and to consider a reconceptualization of childhood disorders in general. It is proposed that the comorbidity found in childhood disorders re¯ects a single underlying etiology: Atypical Brain Development. This de®cit may be manifested in a variety of ways, including DCD, and explains why some childhood disorders are so often seen together. Ó

Although much is known concerning brain-language relations in adults, little is known about how these functions might be represented during the developmental period. We report results from 17 normal children, ages 7-18 years, who have successfully completed a word fluency paradigm during functional magnetic resonance imaging at 3 Tesla. Regions of activation replicate those reported for adult subjects. However, a statistically significant association between hemispheric lateralization of activation and age was found in the children. Specifically, although most subjects at all ages showed left hemisphere dominance for this task, the degree of lateralization increased with age. This study demonstrates that fMRI can reveal developmental shifts in the pattern of brain activation associated with semantic language function.

Epileptic seizures are frequently reported (4-32%) in autism. These values are higher than in the normal population of children and adolescents (0.5%). In the literature there is no uniform description of epilepsy in autism. We examined 106 patients with autistic disorder divided into three groups on the basis of presence or absence of EEG paroxysmal abnormalities (PA) and /or epilepsy including febrile convulsions (FC). Our patients presented an autistic syndrome unrelated to clear congenital or acquired encephalopathy. The prevalence of epilepsy and EEG PA was 23.6% and Hi.%, respectively. Significant differences between the three groups appeared for (8 familial antecedents for epilepsy /FC and neurologic and psychiatric diseases (P < 0.004), (ii) a different proportion between the three groups for mental retardation (P < 0.031, (iii) and EEG fast activity (P < 0.04). Our patients showed several types of epilepsy, including idiopathic forms with seizure onset after the age of 10 in 45% of cases. Seizures were mainly partial, not frequent and controllable by anti-epileptic drugs. PA were mostly focal and multifocal and in 45% of cases were typical of benign childhood partial epilepsy with centro-temporal spikes. The higher incidence of epilepsy and EEG PA is apparently not related to organic pre-, peri-and postnatal antecedents or cerebral lesions. On the contrary, genetic factors responsible for autism and epilepsy seem important in the genesis of these two disorders. 725/644 9053. 0387-7604/95/$09.50 0 1995 Elsevier Science B.V. All rights reserved SSDI 0387-7604(95)00019-4

Aims: Abnormalities of gross motor function in children with autism are well known to clinicians but have not received much empirical documentation and, with the exception of stereotypies, are not among its diagnostic criteria. We recorded the characteristics of gait and prevalence of toe walking, the range of passive joint mobility, and age at walking in children with DSM IV autism spectrum disorders (ASDs) and in age-and gender-matched typically developing peers (mean age 4 years 6 months, range 22 months-10 years 9 months). Methods: We evaluated maximum range of mobility at the elbow, wrist, metacarpo-phalangeal, and ankle joints and videoed children walking and running. Two neurologists blind to diagnosis independently scored features of gait clinically. Results: Children with ASDs had significantly greater joint mobility (p < .002), more gait abnormalities (p < .0001), and on average walked 1.6 months later than their non-autistic peers. Interpretation: This study indicates that attention should be directed to motor abnormalities as well as sociability, communication, and restricted and repetitive behaviors in individuals with ASDs. Motor deficits add to children's other handicaps. They indicate that ASDs affect a broader range of central nervous system circuitry than often appreciated. (I. Rapin).

Neuroscience has provided fascinating glimpses into the brain's development and function. Despite remarkable progress, brain research has not yet been successfully brought to bear in many fields of educational psychology. In this article, work on literacy serves as a test case for an examination of potential future bridges linking mind, brain, and educational psychology. This article proposes a model for integrating research in the cognitive neurosciences with educational psychology and reviews how neuroscience is providing new data relevant to 3 major controversies in the field of dyslexia. This article also discusses the relevance of these findings for psychoeducational assessment and instruction and suggests innovative venues for interdisciplinary research.

The remarkable similarity among the genomes of humans and the African great apes could warrant their classification together as a single genus. However, whereas there are many similarities in the biology, life history, and behavior of humans and great apes, there are also many striking differences that need to be explained. The complete sequencing of the human genome creates an opportunity to ask which genes are involved in those differences. A logical approach would be to use the chimpanzee genome for comparison and the other great ape genomes for confirmation. Until such a great ape genome project can become reality, the next best approach must be educated guesses of where the genetic differences may lie and a careful analysis of differences that we do know about. Our group recently discovered a human-specific inactivating mutation in the CMP-sialic acid hydroxylase gene, which results in the loss of expression of a common mammalian cell-surface sugar throughout all cells in the human body. We are currently investigating the implications of this difference for a variety of issues relevant to humans, ranging from pathogen susceptibility to brain development. Evaluating the uniqueness of this finding has also led us to explore the existing literature on the broader issue of genetic differences between humans and great apes. The aim of this brief review is to consider a listing of currently known genetic differences between humans and great apes and to suggest avenues for future research. The differences reported between human and great ape genomes include cytogenetic differences, differences in the type and number of repetitive genomic DNA and transposable elements, abundance and distribution of endogenous retroviruses, the presence and extent of allelic polymorphisms, specific gene inactivation events, gene sequence differences, gene duplications, single nucleotide polymorphisms, gene expression differences, and messenger RNA splicing variations. Evaluation of the reported findings in all these categories indicates that the CMP-sialic hydroxylase mutation is the only one that has so far been shown to result in a global biochemical and structural difference between humans and great apes. Several of the other known genetic dissimilarities deserve more exploration at the functional level. Among the areas of focus for the future should be genes affecting development, mental maturation, reproductive biology, and other aspects of life history. The approaches taken should include both going from the genome up to the adaptive potential of the organisms and going from novel adaptive regimes down to the relevant repercussions in the genome. Also, as much as we desire a simple genetic explanation for the human phenomenon, it is much more probable that our evolution occurred in multiple genetic steps, many of which must have left detectable footprints in our genomes. Ultimately, we need to know the exact number of genetic steps, the order in which they occurred, and the temporal, spatial, environmental, and cultural contexts that determined their impact on human evolution.

Fish oil remains the main dietary source of long chain polyunsaturated fatty acids omega-3, which desirably impact on human health. Increase of omega-3 fatty acids intake is currently recommended. Results of many studies showed that consumption of food products enriched with fish oil offers the potential health benefits, especially in protection against cardiovascular diseases (CVD), cancer and improvement of brain development and function. Health influence, methods, advantages and disadvantages of food enrichment with fish oil as well as characteristics of market of such products were presented.

An average of 500,000 tons of obsolete Waste Electrical and Electronic Equipments (WEEE) are dumped into Nigeria monthly with its associated health and environmental hazards. E-waste includes computers, entertainment electronics, mobile phones and other items that have been discarded by their original users. While there is no generally accepted definition of e-waste, in most cases e-waste consists of expensive and more or less durable products used for data processing, telecommunications or entertainment in private households and businesses.

Attention deficit hyperactivity disorder (ADHD) has been associated with executive functioning and sustained and divided attention deficits. In order to clarify the questions on neurocognitive impairment in ADHD, we investigated the presence of specific executive functions (EFs) and attention deficit patterns in ADHD clinical subtypes. 50 patients with ADHD and 44 controls were evaluated. All subjects were boys and performed a clinical-psychopathological and neuropsychological battery. Five main domains of EFs and attention were studied. Executive functions-related neurocognitive abilities were used as control tasks. ADHD patients, inattentive and combined subtypes differ from controls on response inhibition, divided attention, phonological, and visual object working memory and on variability of reaction times measured with CPT. Comparison of ADHD subtypes, in five main domains of EFs, did not show evidence of different executive functioning profiles. Response inhibition can predict performance on working memory tests but it cannot predict performance on divided attention/set shifting and on sustained attention. ADHD boys exhibit a selective impairment on executive functions and attention tasks. These data suggest the involvement of partially independent neural circuits which control inhibition and divided attention in ADHD. Since right prefrontal cortex seems to be crucial in controlling response inhibition, while left dorsolateral prefrontal cortex seems important in modulating divided attention, these areas are deputated to be involved in the pathogenesis of neuropsychological deficits in ADHD subtypes. In addition, this study candidates the impairment in phonological and visual-object working memory as a possible neuropsychological trait in ADHD males with inattentive or combined subtypes.

Early severe stress and maltreatment produces a cascade of neurobiological events that have the potential to cause enduring changes in brain development. These changes occur on multiple levels, from neurohumoral (especially the hypothalamic-pituitary-adrenal {HPA} axis) to structural and functional. The major structural consequences of early stress include reduced size of the mid-portions of the corpus callosum and attenuated development of the left neocortex, hippocampus, and amygdala. Major functional consequences include increased electrical irritability in limbic structures and reduced functional activity of the cerebellar vermis. There are also gender differences in vulnerability and functional consequences. The neurobiological sequelae of early stress and maltreatment may play a significant role in the emergence of psychiatric disorders during development.

The assessment of motor functioning in young children has become increasingly important in recent years with the acknowledgement that motor impairment is linked with cognitive, language, social and emotional difficulties. However, there is no one gold standard assessment tool to investigate motor ability in children. The aim of the current paper was to discuss the issues related to the assessment of motor ability in young pre-school children and to provide guidelines on the best approach for motor assessment. The paper discusses the maturational changes in brain development at the preschool level in relation to motor ability. Other issues include sex differences in motor ability at this young age, and evidence for this in relation to sociological versus biological influences. From the previous literature it is unclear what needs to be assessed in relation to motor functioning. Should the focus be underlying motor processes or movement skill assessment? Several key assessment tools are discussed that produce a general measure of motor performance followed by a description of tools that assess specific skills, such as fine and gross motor, ball and graphomotor skills. The paper concludes with recommendations on the best approach in assessing motor function in pre-school children.

The aim of this study was to investigate whether previously observed hypofrontality in adolescents with attention deficit-hyperactivity disorder (ADHD) during executive functioning [Rubia K, Overmeyer S, Taylor E, Brammer M, Williams S, Simmons A, Andrew C, Bullmore ET. Hypofrontality in attention deficit hyperactivity disorder during higher order motor control: a study using fMRI. Am J Psychiatry 1999;156(6):891-896] could be attributed to delayed maturation of frontal cortex. Brain activation of 17 healthy subjects, 9 adolescents and 8 young adults, during performance of a motor response inhibition task and a motor timing task was measured using functional magnetic resonance imaging (fMRI). The effect of age on brain activation was estimated, using the analysis of variance and regression, at both voxel and regional levels. In the delay task, superior performance in adults was paralleled by a significantly increased power of response in a network comprising prefrontal and parietal cortical regions and putamen. In the stop task, alternative neuronal routes -left hemispheric prefrontal regions in adults and right hemispheric opercular frontal cortex and caudate in adolescents -seem to have been recruited by the two groups for achieving comparable performances. A significant age effect was found for the prefrontal activation in both task, confirming the hypothesis of a dysmaturational pathogenesis for the hypofrontality in ADHD. ᭧

Background. Protein encoding genes have long been the major targets for research in schizophrenia genetics. However, with the identification of regulatory microRNAs (miRNAs) as important in brain development and function, miRNAs genes have emerged as candidates for schizophrenia-associated genetic factors. Indeed, the growing understanding of the regulatory properties and pleiotropic effects that miRNA have on molecular and cellular mechanisms, suggests that alterations in the interactions between miRNAs and their mRNA targets may contribute to phenotypic variation. Methodology/Principal Findings. We have studied the association between schizophrenia and genetic variants of miRNA genes associated with brainexpression using a case-control study design on three Scandinavian samples. Eighteen known SNPs within or near brainexpressed miRNAs in three samples (Danish, Swedish and Norwegian: 420/163/257 schizophrenia patients and 1006/177/293 control subjects), were analyzed. Subsequently, joint analysis of the three samples was performed on SNPs showing marginal association. Two SNPs rs17578796 and rs1700 in hsa-mir-206 (mir-206) and hsa-mit-198 (mir-198) showed nominal significant allelic association to schizophrenia in the Danish and Norwegian sample respectively (P = 0.0021 & p = 0.038), of which only rs17578796 was significant in the joint sample. In-silico analysis revealed that 8 of the 15 genes predicted to be regulated by both mir-206 and mir-198, are transcriptional targets or interaction partners of the JUN, ATF2 and TAF1 connected in a tight network. JUN and two of the miRNA targets (CCND2 and PTPN1) in the network have previously been associated with schizophrenia. Conclusions/Significance. We found nominal association between brain-expressed miRNAs and schizophrenia for rs17578796 and rs1700 located in mir-206 and mir-198 respectively. These two miRNAs have a surprising large number (15) of targets in common, eight of which are also connected by the same transcription factors.

Delta (1-4 Hz) EEG power in non-rapid eye movement (NREM) sleep declines massively during adolescence. This observation stimulated the hypothesis that during adolescence the human brain undergoes an extensive reorganization driven by synaptic elimination. The parallel declines in synaptic density, delta wave amplitude and cortical metabolic rate during adolescence further support this model. These late brain changes probably represent the final ontogenetic manifestation of nature's strategy for constructing nervous systems: an initial overproduction of neural elements followed by elimination. Errors in adolescent brain reorganization may cause mental illness; this could explain the typical age of onset of schizophrenia. Longitudinal studies of sleep EEG are enhancing our knowledge of adolescent brain maturation. Our longitudinal study of sleep EEG changes in adolescence showed that delta power, which may reflect frontal cortex maturation, begins its decline between ages 11 and 12 years and falls by 65% by age 17 years. In contrast, NREM theta power begins its decline much earlier. Delta and theta EEG frequencies are important to sleep theory because they behave homeostatically. Surprisingly, these brain changes are unrelated to pubertal maturation but are strongly linked to age. In addition to these (and other) maturational EEG changes, sleep schedules in adolescence change in response to a complex interaction of circadian, social and other influences. Our data demonstrate that the daytime sleepiness that emerges in adolescence is related to the decline in NREM delta as well as to altered sleep schedules. These longitudinal sleep data provide guideposts for studying cognitive and behavioral correlates of adolescent brain reorganization. (I. Feinberg).