Database : MEDLINE
Search on : Autistic and Disorder [Words]
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[PMID]: 29356297
[Au] Autor:Hamed NO; Al-Ayadhi L; Osman MA; Elkhawad AO; Qasem H; Al-Marshoud M; Merghani NM; El-Ansary A
[Ad] Address:Department of Medical Biochemistry, University of Medical Sciences and Technology, Khartoum, Sudan.
[Ti] Title:Understanding the roles of glutamine synthetase, glutaminase, and glutamate decarboxylase autoantibodies in imbalanced excitatory/inhibitory neurotransmission as etiological mechanisms of autism.
[So] Source:Psychiatry Clin Neurosci;, 2018 Jan 22.
[Is] ISSN:1440-1819
[Cp] Country of publication:Australia
[La] Language:eng
[Ab] Abstract:AIM: Autism is a heterogeneous neurological disorder that is characterized by impairments in communication and social interactions, repetitive behaviors, and sensory abnormalities. The etiology of autism remains unclear. Animal, genetic, and post-mortem studies suggest that an imbalance exists in the neuronal excitation and inhibition system in autism. The aim of this study was to determine whether alterations of the measured parameters in children with autism are significantly associated with the risk of a sensory dysfunction. METHODS: The glutamine synthetase (GS), kidney-type glutaminase (GLS1), and glutamic acid decarboxylase autoantibody levels were analyzed in 38 autistic children and 33 age- and sex-matched controls using enzyme-linked immunosorbent assays. RESULTS: The obtained data demonstrated significant alterations in glutamate and glutamine cycle enzymes, as represented by GS and GLS1, respectively. While the glutamic acid decarboxylase autoantibodies levels were remarkably increased, no significant difference was observed compared to the healthy control participants. CONCLUSION: The obtained data indicate that GS and GLS1 are promising indicators of a neuronal excitation and inhibition system imbalance and that combined measured parameters are good predictive biomarkers of autism.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1111/pcn.12639

  2 / 20850 MEDLINE  
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[PMID]: 29520737
[Au] Autor:Lau AA; Tamang SJ; Hemsley KM
[Ad] Address:Childhood Dementia Research Group, Hopwood Centre for Neurobiology, Nutrition and Metabolism Theme, South Australian Health and Medical Research Institute (SAHMRI), PO Box 11060, Adelaide, South Australia, 5001, Australia. adeline.lau@sahmri.com.
[Ti] Title:MPS-IIIA mice acquire autistic behaviours with age.
[So] Source:J Inherit Metab Dis;, 2018 Mar 08.
[Is] ISSN:1573-2665
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Mucopolysaccharidosis (MPS) type IIIA is an inherited, neurodegenerative lysosomal storage disorder resulting from mutations in the SGSH gene. Consequently, N-sulphoglucosamine sulphohydrolase enzyme activity is reduced resulting in impaired catabolism of heparan sulphate. After an asymptomatic period, patients typically show a progressive loss of cognitive and motor skills, with death often during the second decade of life. The diagnostic criteria of autism spectrum disorders (ASD) include impaired communication and social interactions, as well as displays of repetitive behaviours and fixed interests. Children with MPS-IIIA have been shown to exhibit decreased social communicative behaviours from approximately 3-4 years of age but behavioural stereotypies are mostly absent. In this study, we investigated whether a mouse model of MPS-IIIA exhibited ASD-like symptoms. The BTBR T Itpr3 /J inbred mouse model of autism was used as a positive control. Male MPS-IIIA and BTBR mice were less sociable compared with unaffected C57BL/6 male mice in the reciprocal social approach test administered at 20 weeks of age. Alternations in the frequency of social interactions was not evident at earlier stages of the disease course, suggesting an acquisition of ASD-like social behaviours. Stereotypical behaviours were not evident in male MPS-IIIA mice in the marble-burying test nor was the quality of nest constructed by mice affected. Collectively, these data suggest that MPS-IIIA mice acquire autistic social behaviours similar to the human condition, and thus they may be useful for elucidating symptom generating mechanisms and novel treatments for ASD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1007/s10545-018-0160-9

  3 / 20850 MEDLINE  
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[PMID]: 29377098
[Au] Autor:Smith L; Singhal N; El Achkar CM; Truglio G; Rosen Sheidley B; Sullivan J; Poduri A
[Ad] Address:Epilepsy Genetics Program, Department of Neurology, Boston Children's Hospital, Boston, MA, USA.
[Ti] Title:PCDH19-related epilepsy is associated with a broad neurodevelopmental spectrum.
[So] Source:Epilepsia;59(3):679-689, 2018 Mar.
[Is] ISSN:1528-1167
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: To characterize the features associated with PCDH19-related epilepsy, also known as "female-limited epilepsy." METHODS: We analyzed data from participants enrolled in the PCDH19 Registry, focusing on the seizure-related, developmental, neurobehavioral, and sleep-related features. We evaluated variants for pathogenicity based on previous reports, population databases, and in silico predictions, and included individuals with pathogenic or potentially pathogenic variants. We performed a retrospective analysis of medical records and administered a targeted questionnaire to characterize current or past features in probands and genotype-positive family members. RESULTS: We included 38 individuals with pathogenic or potentially pathogenic variants in PCDH19: 21 de novo, 5 maternally inherited, 7 paternally inherited, and 5 unknown. All 38 had epilepsy; seizure burden varied, but typical features of clustering of seizures and association with fever were present. Thirty individuals had intellectual disability (ID), with a wide range of severity reported; notably, 8/38 (22%) had average intellect. Behavioral and sleep dysregulation were prominent, in 29/38 (76%) and 20/38 (53%), respectively. Autistic features were present in 22/38 (58%), of whom 12 had a formal diagnosis of autism spectrum disorder. We had additional data from 5 genotype-positive mothers, all with average intellect and 3 with epilepsy, and from 1 genotype-positive father. SIGNIFICANCE: Our series represents a robust cohort with carefully curated PCDH19 variants. We observed seizures as a core feature with a range of seizure types and severity. Whereas the majority of individuals had ID, we highlight the possibility of average intellect in the setting of PCDH19-related epilepsy. We also note the high prevalence and severity of neurobehavioral phenotypes associated with likely pathogenic variants in PCDH19. Sleep dysregulation was also a major area of concern. Our data emphasize the importance of appropriate referrals for formal neuropsychological evaluations as well as the need for formal prospective studies to characterize the PCDH19-related neurodevelopmental syndrome in children and their genotype-positive parents.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1111/epi.14003

  4 / 20850 MEDLINE  
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[PMID]: 29516460
[Au] Autor:Martinez-Morga M; Quesada-Rico MP; Bueno C; Martinez S
[Ad] Address:Universidad de Murcia, 30071 Murcia, Espana.
[Ti] Title:Bases neurobiologicas del trastorno del espectro autista y del trastorno por deficit de atencion/hiperactividad: diferenciacion neural y sinaptogenesis. [Neurobiological bases of autistic spectrum disorder and attention deficit hyperactivity disorder: neural differentiation and synaptogenesis].
[So] Source:Rev Neurol;66(S01):S97-S102, 2018 Mar 01.
[Is] ISSN:1576-6578
[Cp] Country of publication:Spain
[La] Language:spa
[Ab] Abstract:AIM: To know the neural processes linked to the activity of brain circuits in order to understand the consequences of their dysfunction and their role in the development of neurodevelopmental diseases, such as autistic spectrum disorders (ASD) and attention deficit hyperactivity disorder (ADHD). DEVELOPMENT: The activity of neuronal circuits is the neurobiological basis of behavior and mental activity (emotions, memory and thoughts). The processes of differentiation of neural cells and the formation of circuits by synaptic contacts between neurons (synaptogenesis) occur in the central nervous system during the late stages of prenatal development and the first months after birth. ASD and ADHD share biological features, mainly related to alterations in brain circuits and synaptic function, which allow us to treat them scientifically together. From the neurobiological aspect, ASD and ADHD are manifestations of anomalies in the formation of circuits and synaptic contacts in the brain regions involved in social behavior, and especially in the prefrontal cerebral cortex. These anomalies are caused by mutations in genes involved synaptogenesis and synaptic plasticity, regulation of dendritic spine morphology, synaptic cytoskeletal organization, synthesis and degradation of synaptic proteins, and control of excitatory and inhibitory balance in the synaptic function. CONCLUSIONS: ASD and ADHD are functional alterations of the cerebral cortex, which present structural anomalies in the arrangement of neurons, in the pattern of connections of cortical columns and in the structure of dendritic spines. These alterations affect mainly the prefrontal cortex and its connections.
[Pt] Publication type:CLINICAL CONFERENCE; ENGLISH ABSTRACT
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review

  5 / 20850 MEDLINE  
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[PMID]: 29516452
[Au] Autor:Palau-Baduell M; Salvado-Salvado B; Idiazabal-Alecha MA; Fernandez-Teruel A; Ortiz T
[Ad] Address:Centro de Orientacion y Asistencia al Desarrollo Integral (COADI), Barcelona, Espana.
[Ti] Title:Alteraciones magnetoencefalograficas perisilvianas en pacientes con trastornos del espectro autista. [Perisylvian magnetoencephalografic impairments in patients with autism spectrum disorders].
[So] Source:Rev Neurol;66(S01):S45-S49, 2018 Mar 01.
[Is] ISSN:1576-6578
[Cp] Country of publication:Spain
[La] Language:spa
[Ab] Abstract:INTRODUCTION: The perisylvian areas, located around the Sylvian fissure, are constituted by frontal, temporal and parietal brain regions. These are connected forming specialized neural networks and play a primary role in the development of linguistic skills and social cognition. These areas are a possible neuronal substrate of cognitive and behavioral impairments in patients with autism spectrum disorders (ASD). AIM: To locate and quantify epileptiform activity sources through magnetoencephalography in frontal perisylvian areas in children with idiopathic ASD. PATIENTS AND METHODS: Sixty-eight children with idiopathic ASD were studied by magnetoencephalography. The children were classified into two groups: a group of 41 children with autistic disorder and a combined group of 27 children with Asperger syndrome and children with pervasive developmental disorder not otherwise specified. The sources of magnetoencephalografic epileptiform activity detected in the frontal perisylvian were localized and quantified. RESULTS: The amount of epileptiform activity in frontal perisylvian region was significantly higher in children with autistic disorder. CONCLUSIONS: The amount of epileptiform activity in frontal perisylvian areas differed significantly between children with autistic disorder and those with Asperger syndrome and pervasive developmental disorder not otherwise specified.
[Pt] Publication type:CLINICAL CONFERENCE; ENGLISH ABSTRACT
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review

  6 / 20850 MEDLINE  
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[PMID]: 29516448
[Au] Autor:Ruggieri VL; Arberas CL
[Ad] Address:Hospital Nacional de Pediatria - Prof. Dr. J.P. Garrahan, Buenos Aires, Argentina.
[Ti] Title:Regresion autista: aspectos clinicos y etiologicos. [Autistic regression: clinical and aetiological aspects].
[So] Source:Rev Neurol;66(S01):S17-S23, 2018 Mar 01.
[Is] ISSN:1576-6578
[Cp] Country of publication:Spain
[La] Language:spa
[Ab] Abstract:INTRODUCTION: Autism spectrum disorders are neurodevelopmental dysfunctions that are characterised by deficits in social integration and communication, associated with restricted interests and stereotypic behaviour. A high percentage are related to language disorders, sensory dysfunctions, attention deficit disorder, bipolarity, intellectual disability or epilepsy, among other comorbidities. It is estimated that around 30% of children with autism, with typical early development, may present regression in the first years of life, which was already reported by Kanner in one of his original cases. The term regression refers to the loss of social, communicative or motor skills. It is essential to be alert to any symptoms of autistic regression, since it is not always an unspecific usual manifestation of the clinical spectrum of autism. Although little is known about the pathogenesis of regression, it needs to be organised hierarchically, as it can be part of different conditions with a variety of causes. AIMS: The aim of this study is to analyse distinct conditions that need to be addressed in the case of a child with autistic regression, including genetic and toxic causations, autoimmune and nutritional phenomena, and epilepsies. CONCLUSION: When faced with a case of autistic regression it is essential to try to identify the possible aetiology, as this can allow specific treatment and adequate genetic counselling to be established.
[Pt] Publication type:CLINICAL CONFERENCE; ENGLISH ABSTRACT
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review

  7 / 20850 MEDLINE  
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[PMID]: 29512944
[Au] Autor:Karasawa K; Sano Y; Kato N; Arakawa H
[Ad] Address:Showa University, Tokyo, Japan.
[Ti] Title:Development and clinical application of a bioluminescence enzyme immunoassay for oxytocin.
[So] Source:Luminescence;, 2018 Mar 07.
[Is] ISSN:1522-7243
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The development of a highly sensitive analytical method for oxytocin could be useful in the diagnosis and treatment of autistic spectrum disorder. We previously developed a colorimetric enzyme immunoassay (EIA) for plasma oxytocin measurement. In this study, we developed a method to measure oxytocin concentrations using a higher sensitivity bioluminescent EIA. Biotinylated oxytocin bridged with five lysine residues was used in a competitive format. The standard curve range for oxytocin was 1.0 to 1000 pg/assay. In addition, there was good correlation between the colorimetric and bioluminescent immunoassays in terms of measured oxytocin concentration (r = 0.9665, n = 48). The bioluminescent EIA for plasma oxytocin was more rapid and provided higher sensitivity than the colorimetric immunoassay, making it suitable for clinical application.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher
[do] DOI:10.1002/bio.3462

  8 / 20850 MEDLINE  
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[PMID]: 29512044
[Au] Autor:Geier DA; Kern JK; Sykes LK; Geier MR
[Ad] Address:The Institute of Chronic Illnesses, Inc, 14 Redgate Ct, Silver Spring, MD, USA.
[Ti] Title:Mercury-associated diagnoses among children diagnosed with pervasive development disorders.
[So] Source:Metab Brain Dis;, 2018 Mar 06.
[Is] ISSN:1573-7365
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Nelson and Bauman (Pediatrics 111:674-679, 2003) previously hypothesized that pervasive developmental disorder (PDD) was not associated with mercury (Hg) exposure because the medical conditions associated with Hg exposure were not associated with PDD. A hypothesis-testing longitudinal case-control study evaluated the frequency of medically diagnosed conditions previously associated with Hg poisoning, including: epilepsy, dysarthria, failure to thrive, cerebral palsy, or contact dermatitis and other eczema among children preceding their eventual PDD diagnosis (cases) compared to controls. A retrospective examination of medical records within the Vaccine Safety Datalink (VSD) was undertaken. Cases diagnosed with PDD (n = 534) were born from 1991 to 2000 and continuously enrolled until their PDD diagnosis. Controls (n = 26,367) were born from 1991 to 1993 and continuously enrolled from birth for 7.22 years. Within the first 5 years of life, cases compared to controls were significantly (p < 0.0001) more likely to be assigned a diagnosis of contact dermatitis and other eczema (odds ratio (OR) = 2.033), dysarthria (OR = 23.992), epilepsy (OR = 5.351), failure to thrive (OR = 25.3), and cerebral palsy (OR = 4.464). Similar results were observed when the data were separated by gender. Overall, the results of the present study and recently published studies provide direct evidence supporting a link in twelve of twelve categories (100%) of Hg poisoning associated symptoms as defined by Nelson and Bauman (Pediatrics 111:674-679, 2003) and symptoms observed in those with a PDD diagnosis. The results of this study support the biological plausibility of Hg poisoning to induce PDD diagnoses and rejection of the Nelson and Bauman (Pediatrics 111:674-679, 2003) hypothesis because those with a PDD diagnosis have an increased frequency of conditions previously associated with Hg poisoning.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher
[do] DOI:10.1007/s11011-018-0211-9

  9 / 20850 MEDLINE  
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[PMID]: 29510222
[Au] Autor:Hirsch MM; Deckmann I; Fontes-Dutra M; Bauer-Negrini G; Della-Flora Nunes G; Nunes W; Rabelo B; Riesgo R; Margis R; Bambini-Junior V; Gottfried C
[Ad] Address:Translational Group in Autism Spectrum Disorder - GETTEA, Clinical Hospital of Porto Alegre, RS, Brazil; Department of Biochemistry, Federal University of Rio Grande Do Sul - UFRGS, Porto Alegre, RS, Brazil; Brazilian National Institute of Science and Technology on Neuroimmunomodulation (INCT-NIM),
[Ti] Title:Behavioral alterations in autism model induced by valproic acid and translational analysis of circulating microRNA.
[So] Source:Food Chem Toxicol;, 2018 Mar 03.
[Is] ISSN:1873-6351
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Autism spectrum disorder (ASD) is characterized by difficulties in social interaction, communication and language, and restricted repertoire of activities and interests. The etiology of ASD remains unknown and no clinical markers for diagnosis were identified. Environmental factors, including prenatal exposure to valproic acid (VPA), may contribute to increased risk of developing ASD. MicroRNA (miRNA) are small noncoding RNA that regulate gene expression and are frequently linked to biological processes affected in neurodevelopmental disorders. In this work, we analyzed the effects of resveratrol (an antioxidant and anti-inflammatory molecule) on behavioral alterations of the VPA model of autism, as well as the levels of circulating miRNA. We also evaluated the same set of miRNA in autistic patients. Rats of the VPA model of autism showed reduced total reciprocal social interaction, prevented by prenatal treatment with resveratrol (RSV). The levels of miR134-5p and miR138-5p increased in autistic patients. Interestingly, miR134-5p is also upregulated in animals of the VPA model, which is prevented by RSV. In conclusion, our findings revealed important preventive actions of RSV in the VPA model, ranging from behavior to molecular alterations. Further evaluation of preventive mechanisms of RSV can shed light in important biomarkers and etiological triggers of ASD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180306
[Lr] Last revision date:180306
[St] Status:Publisher

  10 / 20850 MEDLINE  
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[PMID]: 29468499
[Au] Autor:Ahmad SF; Ansari MA; Nadeem A; Alzahrani MZ; Bakheet SA; Attia SM
[Ad] Address:Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh, Kingdom of Saudi Arabia. s_fayazahmad@yahoo.com.
[Ti] Title:Resveratrol Improves Neuroimmune Dysregulation Through the Inhibition of Neuronal Toll-Like Receptors and COX-2 Signaling in BTBR T Itpr3 /J Mice.
[So] Source:Neuromolecular Med;20(1):133-146, 2018 Mar.
[Is] ISSN:1559-1174
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Autism is a neurodevelopmental disorder characterized by deficits in qualitative impairments in communication, repetitive and social interaction, restricted, and stereotyped patterns of behavior. Resveratrol has been extensively studied pharmacologically and biologically and has anti-inflammatory, antioxidant, and neuroprotective effects on neuronal damage in neurodegenerative disorders. The BTBR T Itpr3 /J (BTBR) autistic mouse model has been explored for treatment of autism, which shows low reciprocal social interactions, impaired juvenile play, and decreased social approach. Here, we explored whether resveratrol treatment decreases neuroimmune dysregulation mediated through toll-like receptor (TLR4) and nuclear factor-κB (NF-κB) signaling pathway in BTBR mice. We investigated the effect of resveratrol treatment on TLR2, TLR3, TLR4, NF-κB, and inducible nitric oxide synthase (iNOS or NOS2) levels in CD4 spleen cells. We also assessed the effect of resveratrol treatment on TLR2, TLR3, TLR4, NF-κB, iNOS, and cyclooxygenase (COX-2) mRNA expression levels in the brain tissue. We further explored TLR2, TLR4, NF-κB, iNOS, and COX-2 protein expression levels in the brain tissue. Resveratrol treatment on BTBR mice significantly decreased CD4 TLR2 , CD4 TLR3 , CD4 TLR4 CD4 NF-κB , and CD4 iNOS levels in spleen cells. Resveratrol treatment on BTBR mice decreased TLR2, TLR3, TLR4, NF-κB, iNOS, and COX-2 mRNA expression levels in brain tissue. Moreover, resveratrol treatment resulted in decreased protein expression of TLR2, TLR3, TLR4, NF-κB, iNOS, and COX-2 in brain tissue. Taken together, these results indicate that resveratrol treatment improves neuroimmune dysregulation through the inhibition of proinflammatory mediators and TLRs/NF-κB transcription factor signaling, which might be help devise future therapies for neuroimmune disorders.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:In-Data-Review
[do] DOI:10.1007/s12017-018-8483-0


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