Approaches used to prevent and reduce the use of restrictive practices on adults with learning disabilities: Protocol for a realist review.

INTRODUCTION: The use of restrictive practices has significant adverse effects on the individual, care providers and organisations. This review will describe how, why, for whom, and in what circumstances approaches used by healthcare organisations work to prevent and reduce the use of restrictive practices on adults with learning disabilities. METHODS AND ANALYSIS: Evidence from the literature will be synthesised using a realist review approach - an interpretative, theory-driven approach to understand how complex healthcare approaches work in reducing the use of restrictive practices in these settings. In step 1, existing theories will be located to explore what approaches work by consulting with key topic experts, holding consultation workshops with healthcare professionals, academics, and experts by experience, and performing an informal search to help develop an initial programme theory. A systematic search will be performed in the second step in electronic databases. Further searches will be performed iteratively to test particular subcomponents of the initial programme theory, which will also include the use of the CLUSTER approach. Evidence judged as relevant and rigorous will be used to test the initial programme theory. In step three, data will be extracted and coded inductively and deductively. The final step will involve using a realist logic of analysis to refine the initial programme theory in light of evidence. This will then provide a basis to describe and explain what key approaches work, why, how and in what circumstances in preventing and reducing the use of restrictive practices in adults with learning disabilities in healthcare settings. RESULTS: Findings will be used to provide recommendations for practice and policymaking. REGISTRATION: In accordance with the guidelines, this realist review protocol was registered with the International Prospective Register of Systematic Reviews (PROSPERO) on 4th December 2019 (CRD42019158432).

Temps d'exposition aux écrans et grapho-motricité des enfants de 5 à 6 ans.

PURPOSE OF RESEARCH: To investigate upon the relationship between screen exposure time and graphic/fine motor skills of children aged 5 to 6 in Auvergne. METHODS: A cross-sectional epidemiological study was carried out in 2019-2020 in 3 kindergarten classes in Clermont-Ferrand and 4 in Cantal, chosen according to different socio-demographic criteria. The main criteria for evaluating fine motor skills were 3 calibrated graphic/fine motor activities, carried out during an individual assessment at school. The weekly screen exposure time of the child was assessed during a parental interview. RESULTS: 127 children took part in the survey. The main results point out that children who spend more than 10 hours per school week (more than 20 hours a holiday school week) on screen have significantly lower graphic/fine motor skills. Regardless of screen exposure time, a child living with a single parent, and/or of low level of educational, and/or intermediate occupation/socio-professional category, has lower graphic/fine motor skills scores. The rural setting of the school seems to play a positive role in the level of graphic/fine motor skills, while the socio-demographic profile of the school and the attendance of the children do not seem to influence these skills. CONCLUSIONS: Our survey shows a significant association between increased weekly screen time exposure and decreased graphic/fine motor skills in children aged 5-6 years. Further work will be required to explore this association. Health education programs implemented in school and health communities with parental involvement would be useful to improve screen usage and prevent learning disabilities.

Melatonin protects against methamphetamine-induced Alzheimer's disease-like pathological changes in rat hippocampus.

Methamphetamine (METH) is a psychostimulant drug of abuse. METH use is associated with cognitive impairments and neurochemical abnormalities comparable to pathological changes observed in Alzheimer's disease (AD). These observations have stimulated the idea that METH abusers might be prone to develop AD-like signs and symptoms. Melatonin, the pineal hormone, is considered as a potential therapeutic intervention against AD. We thus conducted the present study to explore potential protective roles of melatonin against METH-induced deficits in learning and memory as well as in the appearance of AD-like pathological changes in METH-treated male Wistar rats. We found that melatonin ameliorated METH-induced cognitive impairments in those rats. Melatonin prevented METH-induced decrease in dopamine transporter (DAT) expression in rat hippocampus. Melatonin reversed METH-induced activation of ß-arrestin2, reduction of phosphorylation of protein kinase B (Akt) and METH-induced excessive activity of glycogen synthase kinase-3ß (GSK3ß). Importantly, melatonin inhibited METH-induced changes in the expression of ß-site APP cleaving enzyme (BACE1), disintegrin and metalloproteinase 10 (ADAM10), and presenilin 1 (PS1), as well as the reduction of amyloid beta (Aß)42 production. Immunofluorescence double-labeling demonstrated that melatonin not only prevented the METH-induced loss of DAT but also prevented METH-induced Aß42 overexpression in the dentate gyrus, CA1, and CA3. Furthermore, melatonin also suppressed METH-induced increase in phosphorylated tau. Significantly, melatonin attenuated METH-induced increase in N-methyl-D-aspartate receptor subtype 2 B (NR2B) protein expression and restored METH-induced reduction of Ca2+/calmodulin-dependent protein kinase II (CaMKII). This suggested that melatonin attenuated the toxic effect of METH on the hippocampus involving the amyloidogenic pathway. Taken together, our data suggest that METH abuse may be a predisposing risk factor for AD and that melatonin could serve as a potential therapeutic agent to prevent METH-induced AD like pathology.

Aversive Learning Deficits and Depressive-Like Behaviors Are Accompanied by an Increase in Oxidative Stress in a Rat Model of Fetal Alcohol Spectrum Disorders: The Protective Effect of Rapamycin.

Fetal alcohol spectrum disorders (FASDs) are one of the most common consequences of ethanol exposure during pregnancy. In adulthood, these disorders can be manifested by learning and memory deficits and depressive-like behavior. Ethanol-induced oxidative stress may be one of the factors that induces FASD development. The mammalian target of the Rapamycin (mTOR) signaling pathway that acts via two distinct multiprotein complexes, mTORC1 and mTORC2, can affect oxidative stress. We investigated whether mTOR-dependent or mTOR-independent mechanisms are engaged in this phenomenon. Thus, Rapamycin-a selective inhibitor of mTORC1, Torin-2-a non-selective mTORC1/mTORC2 inhibitor, and FK-506-a drug that impacts oxidative stress in an mTOR-independent manner were used. Behavioral tests were performed in adult (PND60-65) rats using a passive avoidance (PA) task (aversive learning and memory) and forced swimming test (FST) (depressive-like behaviors). In addition, the biochemical parameters of oxidative stress, such as lipid peroxidation (LPO), as well as apurinic/apyrimidinic (AP)-sites were determined in the hippocampus and prefrontal cortex in adult (PND65) rats. The rat FASD model was induced by intragastric ethanol (5 g/kg/day) administration at postnatal day (PND)4-9 (an equivalent to the third trimester of human pregnancy). All substances (3 mg/kg) were given 30 min before ethanol. Our results show that neonatal ethanol exposure leads to deficits in context-dependent fear learning and depressive-like behavior in adult rats that were associated with increased oxidative stress parameters in the hippocampus and prefrontal cortex. Because these effects were completely reversed by Rapamycin, an mTORC1 inhibitor, this outcome suggests its usefulness as a preventive therapy in disorders connected with prenatal ethanol exposure.

The ketogenic diet raises brain oxygen levels, attenuates postictal hypoxia, and protects against learning impairments.

OBJECTIVES: A prolonged vasoconstriction/hypoperfusion/hypoxic event follows self-terminating focal seizures. The ketogenic diet (KD) has demonstrated efficacy as a metabolic treatment for intractable epilepsy and other disorders but its effect on local brain oxygen levels is completely unknown. This study investigated the effects of the KD on tissue oxygenation in the hippocampus before and after electrically elicited (kindled) seizures and whether it could protect against a seizure-induced learning impairment. We also examined the effects of the ketone ß-hydroxybutyrate (BHB) as a potential underlying mechanism. METHODS: Male and female rats were given access to one of three diet protocols 2 weeks prior to the initiation of seizures: KD, caloric restricted standard chow, and ad libitum standard chow. Dorsal hippocampal oxygen levels were measured prior to initiation of diets as well as before and after a 10-day kindling paradigm. Male rats were then tested on a novel object recognition task to assess postictal learning impairments. In a separate cohort, BHB was administered 30 min prior to seizure elicitation to determine whether it influenced oxygen dynamics. RESULTS: The KD increased dorsal hippocampal oxygen levels, ameliorated postictal hypoxia, and prevented postictal learning impairments. Acute BHB administration did not alter oxygen levels before or after seizures. INTERPRETATION: The ketogenic diet raised brain oxygen levels and attenuated severe postictal hypoxia likely through a mechanism independent of ketosis and shows promise as a non-pharmacological treatment to prevent the postictal state.

Development of an Eco-Biodevelopmental Model of Emergent Literacy Before Kindergarten: A Review.

Importance: Literacy has been described as an important social determinant of health. Its components emerge in infancy and are dependent on genetic, medical, and environmental factors. The American Academy of Pediatrics advocates a substantial role for pediatricians in literacy promotion, developmental surveillance, and school readiness to promote cognitive, relational, and brain development. Many children, especially those from minority and underserved households, enter kindergarten unprepared to learn to read and subsequently have difficulty in school. Observations: Emergent literacy is a developmental process beginning in infancy. Component skills are supported by brain regions that must be adequately stimulated and integrated to form a functional reading network. Trajectories are associated with genetic, medical, and environmental factors, notably the home literacy environment, which is defined as resources, motivation, and stimulation that encourage the literacy development process. Eco-biodevelopmental models are advocated by the American Academy of Pediatrics, and these models offer insights into the neurobiological processes associated with environmental factors and the ways in which these processes may be addressed to improve outcomes. Emergent literacy is well suited for such a model, particularly because the mechanisms underlying component skills are elucidated. In addition to cognitive-behavioral benefits, the association of home literacy environment with the developing brain before kindergarten has recently been described via neuroimaging. Rather than a passive approach, which may subject the child to stress and engender negative attitudes, early literacy screening and interventions that are administered by pediatric practitioners can help identify potential reading difficulties, address risk factors during a period when neural plasticity is high, and improve outcomes. Conclusions and Relevance: Neuroimaging and behavioral evidence inform an eco-biodevelopmental model of emergent literacy that is associated with genetic, medical, and home literacy environmental factors before kindergarten, a time of rapid brain development. This framework is consistent with recommendations from the American Academy of Pediatrics and provides insights to help identify risk factors and signs of potential reading difficulties, tailor guidance, and provide direction for future research.

Neuroprotective effect of Betalain against AlCl3-induced Alzheimer's disease in Sprague Dawley Rats via putative modulation of oxidative stress and nuclear factor kappa B (NF-κB) signaling pathway.

Alzheimer's disease (AD) is the most progressive form of neurodegenerative disease, which severely impairs cognitive function. Oxidative stress is identified to contribute to the mechanisms responsible for the pathogenesis of such neurodegenerative diseases. Aluminum is a potent neurotoxin for inducing oxidative stress associated with neurodegenerative diseases. The treatment for AD is limited; hence more treatment options are the need of the day. Betalain is known for its multitude of medicinal assets, including anti-inflammatory activity. Hence, this study was intended to investigate the possible protective effect of betalain against aluminum chloride (AlCl3) induced AD on Sprague Dawley (SD) rats. AlCl3 (100 mg/kg) was administrated orally to induce the AD in SD rats. The rats were supplemented with low and high betalain doses (10 mg/kg and 20 mg/kg) for four weeks. At the end of the experiment, the rats were subjected to behavioral examination and sacrificed to study the biochemical and histological parameters. The results showed attenuation of memory and learning capacity, suppression of lipid oxidation (MDA) through regulation of antioxidant content (SOD, CAT, and GSH) and inhibition of lactate dehydrogenase (LDH), nitric oxide (NO), acetylcholinesterase (AChE), and transmembrane protein (Na+K+ATPase) activity. In addition, the NF-ƙB associated mRNA expression (TNF-α IL-6, Il-1ß, iNOS, COX-2) was decreased, as evidenced in histopathological results. The present investigation established that the betalain treatment ameliorated the AlCl3 induced AD by modulating NF-κB pathway activation.

Imidazopyridine-Based 5-HT6 Receptor Neutral Antagonists: Impact of N1-Benzyl and N1-Phenylsulfonyl Fragments on Different Receptor Conformational States.

G-protein coupled receptors (GPCRs) exist in an equilibrium of multiple conformational states, including different active states, which depend on the nature of the bound ligand. In consequence, different conformational states can initiate specific signal transduction pathways. The study identified compound 7e, which acts as a potent 5-hydroxytryptamine type 6 receptor (5-HT6R) neutral antagonist at Gs and does not impact neurite growth (process controlled by Cdk5). MD simulations highlighted receptor conformational changes for 7e and inverse agonist PZ-1444. In cell-based assays, neutral antagonists of the 5-HT6R (7e and CPPQ), but not inverse agonists (SB-258585, intepirdine, PZ-1444), displayed glioprotective properties against 6-hydroxydopamine-induced and doxorubicin-induced cytotoxicity. These suggest that targeting the activated conformational state of the 5-HT6R with neutral antagonists implicates the protecting properties of astrocytes. Additionally, 7e prevented scopolamine-induced learning deficits in the novel object recognition test in rats. We propose 7e as a probe for further understanding of the functional outcomes of different states of the 5-HT6R.

Pediatric Obstructive Sleep Apnea and Neurocognition.

Pediatric obstructive sleep apnea affects a large number of children and has multiple end-organ sequelae. Although many of these have been demonstrated to be reversible, the effects on some of the organ systems, including the brain, have not shown easy reversibility. Progress in this area has been hampered by lack of a preclinical model to study the disease. Therefore, perioperative and sleep physicians are tasked with making a number of difficult decisions, including optimal surgical timing to prevent disease evolution, but also to keep the perioperative morbidity in a safe range for these patients.

A Snapshot of RTI Implementation a Decade Later: New Picture, Same Story.

Response to intervention (RTI) has evolved from its first decade of implementation. Because states guide and regulate policy and practice at the state and local education agency levels, it is important to understand their critical role in RTI implementation. A systematic review of all 50 state education agency websites was conducted to provide an updated "snapshot" of states' interpretation of RTI a decade after IDEA regulations were finalized. Findings revealed substantive progress towards developing approaches to systematic supports to students, with a major trend in adoption of multi-tiered system of support (MTSS) models. Findings also documented continued variation in how states are communicating about tiered systems on such matters as the roles of tiered systems in schoolwide prevention frameworks, meeting special education requirements, and aligning multiple systems within schools. Implications for special education services for students with learning disabilities are discussed.

Quercetin ameliorates diabetic encephalopathy through SIRT1/ER stress pathway in db/db mice.

Studies have shown that diabetes is an important risk factor for cognitive dysfunction, also called diabetic encephalopathy (DE). Quercetin has been reported to be effective in improving cognitive dysfunction in DE. But its detailed mechanism is still ambiguous. In this study, we used db/db mice to investigate whether quercetin could activate SIRT1 and inhibit ER pathways to improve DE. Behavioral tests (Morris water maze and new objects) showed that quercetin (70 mg/kg) can effectively improve the learning and memory ability in db/db mice. OGTT and ITT tests indicated that quercetin could alleviate impaired glucose tolerance and insulin resistance in db/db mice. Western blot analysis and Nissl staining showed that quercetin can improve the expression of nerve and synapse-associated proteins (PSD93, PSD95, NGF and BDNF) and inhibit neurodegeneration. Meanwhile, quercetin up-regulates SIRT1 protein expression and inhibits the expression of ER signaling pathway-related proteins (PERK, IRE-1α, ATF6, eIF2α, BIP and PDI). In addition, oxidative stress levels were significantly reduced after quercetin treatment. In conclusion, current experimental results indicated that SIRT1/ER stress is a promising mechanism involved in quercetin-treated diabetic encephalopathy.

Sirtuin 2 Inhibition Attenuates Sevoflurane-Induced Learning and Memory Deficits in Developing Rats via Modulating Microglial Activation.

Sevoflurane is a widely used inhalational anesthetic in pediatric medicine that has been reported to have deleterious effects on the developing brain. Strategies to mitigate these detrimental effects are lacking. Sirtuin 2 (SIRT2) is a member of nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylases involved in a wide range of pathophysiological processes. SIRT2 inhibition has emerged as a promising treatment for an array of neurological disorders. However, the direct effects of SIRT2 on anesthesia-induced damage to the immature brain are unclear. Neonatal rats were exposed to 3% sevoflurane or 30% oxygen for 2 h daily with or without SIRT2 inhibitor AK7 pretreatment from postnatal day 7 (P7) to P9. One cohort of rats were euthanized 6, 12, and/or 24 h after the last gas exposure, and brain tissues were harvested for biochemical analysis and/or immunohistochemical examination. Cognitive functions were evaluated using the open field and Morris water maze tests on P25 and P28-32, respectively. SIRT2 was significantly up-regulated in neonatal rat hippocampus at 6 and 12 h post-anesthesia. Pretreatment with SIRT2 inhibitor AK7 reversed sevoflurane-induced hippocampus-dependent cognitive impairments. Furthermore, AK7 administration mitigated sevoflurane-induced neuroinflammation and microglial activation. Concomitantly, AK7 inhibited pro-inflammatory/M1-related markers and increased anti-inflammatory/M2-related markers in microglia. AK7 might prevent sevoflurane-induced neuroinflammation by switching microglia from the M1 to M2 phenotype. Downregulation of SIRT2 may be a novel therapeutic target for alleviating anesthesia-induced developmental neurotoxicity.

School-aged Children Who Are Not Progressing Academically: Considerations for Pediatricians.

Pediatricians and other pediatric primary care providers may be consulted when families have concerns that their child is not making expected progress in school. Pediatricians care not only for an increasingly diverse population of children who may have behavioral, psychological, and learning difficulties but also for increasing numbers of children with complex and chronic medical problems that can affect the development of the central nervous system and can present with learning and academic concerns. In many instances, pediatric providers require additional information about the nature of cognitive, psychosocial, and educational difficulties that affect their school-aged patients. Our purpose for this report is to describe the current state of the science regarding educational achievement to inform pediatricians' decisions regarding further evaluation of a child's challenges. In this report, we review commonly available options for psychological evaluation and/or treatment, medical referrals, and/or recommendations for referral for eligibility determinations at school and review strategies for collaborating with families, schools, and specialists to best serve children and families.

Neuroprotective effects of lipopolysaccharide and naltrexone co­preconditioning in the photothrombotic model of unilateral selective hippocampal ischemia in rat.

Preconditioning with lipopolysaccharide (LPS) or opioid antagonists has a neuroprotective effect in ischemic insults. However, the co­preconditioning effect of toll­like receptor ligands and opioid antagonists has not been investigated. In this study we examined the neuroprotective effect of LPS and naltrexone (NTX) preconditioning and co­preconditioning in unilateral selective hippocampal ischemia in rats to assess for possible synergistic protective effects. LPS and NTX were injected unilaterally into the left cerebral ventricle of male rats. Forty­eight hours after LPS and twenty­four hours after NTX injection, ipsilateral selective hippocampal ischemia was induced using a modified version of the photothrombotic method. Protective effects for LPS and NTX were assessed by evaluating infarct volume (using 2,3,5­triphenyltetrazolium chloride staining), and cognitive function (using radial arm water maze and passive avoidance tests). Animals in the ischemic group had an infarct lesion and considerable cognitive impairment, compared with the sham group. LPS or NTX preconditioning significantly reduced the infarct size and improved cognitive function. Moreover, co­preconditioning with LPS and NTX increased the protective effect compared with preconditioning with LPS or NTX alone. Our data showed that LPS and NTX preconditioning resulted in a neuroprotective effect in hippocampal ischemia. Furthermore, co­preconditioning with LPS and NTX resulted in a synergistic protective effect.

Antidepressant and Neuroprotective Effects of Naringenin via Sonic Hedgehog-GLI1 Cell Signaling Pathway in a Rat Model of Chronic Unpredictable Mild Stress.

Depression is one of the most prevalent and crucial public health problem connected to significant mortality and co-morbidity. Recently, numerous studies suggested that dietary flavanones exhibit neuroprotective and antidepressant effects against various psycho-physiological conditions including depression. The present study is focused on the antidepressant and neuroprotective effects of naringenin (NAR) and the involvement of sonic hedgehog (Shh) signaling in the chronic unpredictable mild stress (CUMS)-induced depression. Twenty-four male Wistar rats were randomly assigned into four groups: CON group (saline s.c.), NAR group (NAR 50 mg/kg, p.o.), CUMS group (subjected to CUMS along with saline p.o.), and CUMS + NAR group (NAR 50 mg/kg p.o. along with CUMS) for 28 days including 1-week pre-treatment with NAR. The results showed that NAR was found to inhibit behavioral abnormalities including increased despair in force swim test, and reduced locomotor activity caused by CUMS in open field test. Moreover, Morris water maze revealed that NAR also mitigates CUMS-associated cognitive impairment. In addition to the antidepressant-like effect, NAR mitigates morphological anomalies in the hippocampal CA1 region and cortex. Furthermore, we observed brain-derived neurotrophic factor (BDNF), Shh, GLI1, NKX2.2, and PAX6 were downregulated in the hippocampus of CUMS-exposed rats, which can be upregulated by NAR pre-treatment. GLI1 is main downstream signaling component of Shh signaling cascade, which further regulates the expression of homeodomain transcription factors PAX6 and NKX2.2.

Resveratrol prevents high-calorie diet-induced learning and memory dysfunction in juvenile C57BL/6J mice.

OBJECTIVE: Because resveratrol (RSV) has been shown to improve learning and memory, so we investigated the potential benefit of RSV on learning and memory deficits in juvenile mice fed with a HC diet and explored the molecular mechanisms underlying this process. METHODS: Six-week-old C57BL/6J mice were divided into three different diet groups: control, HC diet, and HC + RSV diet. Serum insulin and insulin-like growth factor 1 (IGF-1) levels were measured using enzyme-linked immunosorbent assays. Protein expression was examined by immunohistochemistry and western blotting. RESULTS: Administration of RSV daily (30 mg/kg) prevented the HC diet-induced increase in juvenile animal body weight but did not improve any other physiological conditions, including fasting blood glucose and serum cholesterol, triglyceride, insulin, and IGF-1 levels. However, RSV did prevent learning and memory deficits in the HC group. Peroxisome proliferator-activated receptor gamma (PPARγ) was downregulated in the CA1 region of the hippocampus in both the HC and HC + RSV groups, but the reduction was significantly greater in the HC + RSV group (P < .01 compared with the HC group). Moreover, although the HC diet reduced the number of p16-positive neurons, the HC + RSV diet significantly upregulated p16 expression in the CA1 region of the hippocampus (P < .01 compared with the HC group). CONCLUSIONS: RSV protected against learning and memory impairments in juvenile animals fed with a HC diet, possibly via upregulation of p16 or downregulation of PPARγ in the hippocampal CA1 region.

Calmodulin-like skin protein protects against spatial learning impairment in a mouse model of Alzheimer disease.

Humanin and calmodulin-like skin protein (CLSP) inhibits Alzheimer disease (AD)-related neuronal cell death via the heterotrimeric humanin receptor in vitro. It has been suggested that CLSP is a central agonist of the heterotrimeric humanin receptor in vivo. To investigate the role of CLSP in the AD pathogenesis in vivo, we generated mouse CLSP-1 transgenic mice, crossed them with the APPswe/PSEN1dE9 mice, a model mouse of AD, and examined the effect of CLSP over-expression on the pathological phenotype of the AD mouse model. We found that over-expression of the mouse CLSP-1 gene attenuated spatial learning impairment, the loss of a presynaptic marker synaptophysin, and the inactivation of STAT3 in the APPswe/PSEN1dE9 mice. On the other hand, CLSP over-expression did not affect levels of Aß, soluble Aß oligomers, or gliosis. These results suggest that the CLSP-mediated attenuation of memory impairment and synaptic loss occurs in an Aß-independent manner. The results of this study may serve as a hint to the better understanding of the AD pathogenesis and the development of AD therapy.

Influences of early child nutritional status and home learning environment on child development in Vietnam.

Early childhood development plays a key role in a child's future health, educational success, and economic status. However, suboptimal early development remains a global challenge. This study examines the influences of quality of the home learning environment (HOME) and child stunting in the first year of life on child development. We used data collected from a randomized controlled trial of preconceptional micronutrient supplementation in Vietnam (n = 1,458). The Bayley Scales of Infant Development-III were used to assess cognition, language, and motor development domains at 2 years. At 1 year, 14% of children were stunted, and 15%, 58%, and 28% of children lived in poor, medium, and high HOME environments, respectively. In multivariate generalized linear regression models, living in a high HOME environment was significantly associated with higher scores (0.10 to 0.13 SD) in each of the developmental domains. Stunted children scored significantly lower for cognitive, language, and motor development (-0.11 to -0.18), compared to nonstunted children. The negative associations between stunting on development were modified by HOME; the associations were strong among children living in homes with a poor learning environment whereas they were nonsignificant for those living in high-quality learning environments. In conclusion, child stunting the first year of life was negatively associated with child development at 2 years among children in Vietnam, but a high-quality HOME appeared to attenuate these associations. Early interventions aimed at improving early child growth as well as providing a stimulating home environment are critical to ensure optimal child development.

n-3 Polyunsaturated fatty acid supplementation restored impaired memory and GABAergic synaptic efficacy in the hippocampus of stressed rats.

While chronic stress induces dendritic atrophy in the hippocampus and impairs learning and memory, supplementation with n-3 polyunsaturated fatty acids (n-3 PUFA) is known to improve learning and memory of control rats. Whether n-3 PUFA supplementation improves dendritic morphology, synaptic transmission, and memory of chronically stressed rats remains unknown. In this work, we randomly assigned male Sprague-Dawley rats in four experimental groups: two unsupplemented groups, control and stress, and two supplemented groups with n-3 PUFA (DHA and EPA mix), control + n-3 PUFA and stress + n-3 PUFA. Dendritic morphology and synaptic transmission in the hippocampus were evaluated by Golgi stain and patch-clamp tools, respectively. The Y-maze and Morris water maze were used to analyze the effects of chronic stress on memory. Supplementation with n-3 PUFA improved dendritic architecture and restored the frequency of inhibitory post-synaptic currents of hippocampal pyramidal neurons of rats from stress group. In addition, n-3 PUFA supplementation improved spatial memory. Our results demonstrate that n-3 PUFA supplementation had three beneficial effects on stressed rats: prevented or compensated dendritic atrophy in CA3; restored the probability of GABA release in CA1; and improved spatial memory. We argue that n-3 PUFA supplementation can be used in treating stress-related psychiatric disorders such as depression and anxiety.

Effects of a working memory training program in preschoolers with symptoms of attention-deficit/hyperactivity disorder.

INTRODUCTION: Preschoolers with attention-deficit/hyperactivity disorder (ADHD) have been found to exhibit impairments on neuropsychological measures of working memory (WM). As WM is an important predictor of future learning abilities, early intervention could help to prevent severe problems. The purpose of this research was to ascertain the efficacy of an intervention for training WM in 5-year-old children with symptoms of ADHD. METHOD: Thirty-four children with symptoms of ADHD were randomly divided into two groups: One was assigned to the WM training condition, and the other continued normal class activities. The training was provided at school in small groups that also included typically developing children. RESULTS: The trained group showed a significant improvement in tasks measuring their WM and other controlled processes at conclusion of study, whereas no significant improvement was found in the control group. CONCLUSIONS: We concluded that early intervention on WM may be effective in children with symptoms of ADHD.