Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004352 (autism)
 32,579 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Katz (1978) has suggested that mild, fluctuating conductive hearing loss due to middle-ear anomalies may account for the language and attention problems of learning-disabled children. His position was extended here to include autism. Normal, learning-disabled, and autistic children received repeated impedance measures over 5 weeks. A repeated-measures ANOVA of central tendency and variability values led to the conclusions that (1) fluctuating, negative middle-ear pressure greater than normal characterizes both autistic and learning-disabled children, (2) the negative pressure is greater in autistic than in learning-disabled children, and (3) the condition is typically bilateral for autistic children.
J Autism Dev Disord 1988 Mar
PMID:Conductive hearing loss in autistic, learning-disabled, and normal children. 337 59

The present study was conducted to determine whether certain stimulus conditions were associated with high and low rates of autistic children's self-stimulation. Six autistic boys were assessed in situations varying along three dimensions: familiarity or unfamiliarity of setting, learning task, and therapist. Each child was observed in 10 10-min stimulus conditions, and trained observers recorded the occurrence of self-stimulation within each condition. The results of a 2 x 2 x 2 ANOVA indicated that self-stimulation occurred significantly more often with an unfamiliar than with a familiar therapist. Unfamiliar versus familiar setting and task were not significant effects, and there were no significant interactions. Also, significant differences were found within each condition, with self-stimulation increasing in frequency as the sessions progressed. Finally, there was a significant and negative correlation between the occurrence of self-stimulation and correct responding. These findings suggest several treatment strategies for facilitating a generalized suppression of autistic children's self-stimulation.
J Autism Dev Disord 1986 Mar
PMID:The occurrence of autistic children's self-stimulation as a function of familiar versus unfamiliar stimulus conditions. 395 57

1. Serum serotonin (5HT) was determined in normal and autistic children by high performance liquid chromatography with electrochemical detection (HPLC-ED), after serum deproteinization. 2. The sample deproteinization was carried out by the addition of 3.4 M HCLO4 to a small volume of the serum, followed by freezing, centrifugation, dilution and injection of sample into the HPLC. 3. Serum 5HT concentration was significantly increased in autistic children (303 +/- 92 ng/ml) (N = 19) when compared to that of normal children (215 +/- 67 ng/ml) (N = 46). The data of normal children analyzed by ANOVA for sex or age showed no difference. 4. The method employed in this study showed high resolution, good sensitivity and can be used for routine determination of serum 5HT in the clinical investigation of hyperserotonemia in autism.
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PMID:Serum serotonin levels of normal and autistic children. 825 30

To clarify the pathophysiology of learning disability (LD), we measured the urinary levels of 3-methoxy-4-hydroxyphenyl glycol (MHPG), and phenylethylamine (PEA) in urine samples collected in a 24 hour period. Findings were compared with those obtained in age-matched controls and diseased controls including patients with attention deficit-hyperactivity disorder (ADHD), infantile autism, and mental retardation. The mean urinary level of MHPG in LD (n = 6) were not significantly different from those in ADHD (n = 16), mental retardation (n = 4), infantile autism (n = 5), and the controls (n = 6), while the mean urinary levels of PEA were significantly lower in LD (n = 6, 91 +/- 17.3 micrograms/mg) and in ADHD (n = 5, 65 +/- 53.6 micrograms/mg) as compared to age-matched controls (n = 3, 340 +/- 264.5 micrograms/mg) ANOVA, (p < 0.05). PEA is considered to play an important role for the pathogenesis of LD and ADHD.
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PMID:[Neurochemical and neurotransmitter studies in patients with learning disabilities]. 1035 64

There has been little exploration of major biologic regulators of cerebral development in autism. In archived neonatal blood of children with autistic spectrum disorders (n = 69), mental retardation without autism (n = 60), or cerebral palsy (CP, n = 63) and of control children (n = 54), we used recycling immunoaffinity chromatography to measure the neuropeptides substance P (SP), vasoactive intestinal peptide (VIP), pituitary adenylate cyclase-activating polypeptide (PACAP), calcitonin gene-related peptide (CGRP), and the neurotrophins nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4/5 (NT4/5). Neonatal concentrations of VIP, CGRP, BDNF, and NT4/5 were higher (ANOVA, all p values < 0.0001 by Scheffe test for pairwise differences) in children in the autistic spectrum and in those with mental retardation without autism than in control children. In 99% of children with autism and 97% with mental retardation, levels of at least one of these substances exceeded those of all control children. Concentrations were similar in subgroups of the autistic spectrum (core syndrome with or without mental retardation, other autistic spectrum disorders with or without mental retardation) and in the presence or absence of a history of regression. Among children with mental retardation, concentrations did not differ by severity or known cause (n = 11, including 4 with Down syndrome). Concentrations of measured substances were similar in children with CP as compared with control subjects. SP, PACAP, NGF, and NT3 were not different by diagnostic group. No measured analyte distinguished children with autism from children with mental retardation alone. In autism and in a heterogeneous group of disorders of cognitive function, overexpression of certain neuropeptides and neurotrophins was observed in peripheral blood drawn in the first days of life.
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PMID:Neuropeptides and neurotrophins in neonatal blood of children with autism or mental retardation. 1135 50

A polymorphic trinucleotide repeat (CGG/GCC) within the human Reelin gene (RELN) was examined as a candidate gene for autism spectrum disorders (ASDs). This gene encodes a large extracellular matrix protein that orchestrates neuronal positioning during corticogenesis. The CGG-repeat within the 5' untranslated region of RELN exon 1 was examined in 126 multiple-incidence families. The number of CGG repeats varied from three to 16 in affected individuals and controls, with no expansion or contraction observed during maternal (n = 291) or paternal (n = 287) transmissions in families with autistic probands. Although the frequencies of the RELN alleles and genotypes in affected children were not different from those in the comparison group, a family-based association test (FBAT) showed that the larger RELN alleles (> or = 11 repeats) were transmitted more often than expected to affected children (S = 43, E(S) = 34.5, P = 0.035); this was particularly the case for the 13-repeat RELN allele (S = 22, E(S) = 16, P = 0.034). Affected sib-pair (ASP) analysis found no evidence of excess sharing of RELN alleles in affected siblings. The impact of genotypes with large alleles (> or = 11 repeats) on the phenotypes in individuals with ASD was analyzed by ANOVA in a subset of the families for which results of the Autism Diagnostic Interview-Revised were available. Children with large RELN alleles did not show any difference in scores for questions related to the core symptoms of autistic disorder, but there was a tendency for children with at least one large RELN allele to have an earlier age at first phrase (chi(2) = 3.538, P = 0.06). Thus, although the case-control and affected sib-pair findings did not support a role for RELN in susceptibility to ASD, the more powerful family-based association study demonstrated that RELN alleles with larger numbers of CGG repeats may play a role in the etiology of some cases of ASD, especially in children without delayed phrase speech.
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PMID:Reelin gene alleles and susceptibility to autism spectrum disorders. 1239 38

In this study, we longitudinally followed into childhood a cohort of preschool children, initially diagnosed as autistic or non-autistic with developmental delay, to evaluate the stability of cognitive assessments performed during the preschool period. The consistency in group means and intra-individual stability of developmental quotients (DQ) and non-verbal intelligence quotients (IQs) were compared for these two groups, which were matched by chronological age, initial non-verbal IQ/DQs, initial test given, and length of follow-up interval. The case group comprised 16 autistic children with average age at initial assessment of 3 years 8 months. The control group comprised 16 non-autistic developmental delayed children with average age at initial assessment of 3 years 11 months. Mean DQ/non-verbal IQ at initial assessment was 73.9+/-23.9 for the case group and 80.3+/-23.2 for the control group. ANOVA yielded no significant effect of time or time x diagnosis interaction (F=0.183, P=0.675). The absolute difference in scores and group means were equivalent for both groups of children, with no difference in patterns of change. Correlations between DQ/non-verbal IQs at initial assessment and follow-up were significant and high for the two groups (autistic group: r=0.87; control: r=0.77). Intellectual functioning can be a valid measure in Taiwanese preschool children with autism, and has an equivalent meaning for children with autism and for non-autistic children with developmental delay. Though the follow-up period is too short for definite prognostic conclusions to be drawn, we think that non-verbal intelligence should be an essential assessment for preschool oriental autistic children so that sound expectation and treatment plan can be made.
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PMID:Preschool children with autism spectrum disorders in Taiwan: follow-up of cognitive assessment to early school age. 1458 Jun 67

To report on the cognitive and behavioral attributes of 61 children with Down syndrome (DS) and autistic-spectrum disorder (ASD) according to DSM-IV criteria; to determine the utility of the aberrant behavior checklist (ABC) to characterize these subjects for research purposes; and to test the hypothesis that subjects with DS + ASD could be distinguished from their typical DS peers using the ABC. Cross-sectional design. Cases with DS + ASD (N = 61), comparison group of DS + stereotypy movement disorder (SMD) (N = 26) and typical DS controls without behavior problems (N = 44) were ascertained and enrolled sequentially upon presentation to a DS clinic at an academic medical center over a 10-year period from 1991 to 2001. All subjects underwent neurodevelopmental and medical evaluation, and standardized cognitive testing. The parents provided responses to standardized behavioral questionnaires. Cognitive function (IQ) differed markedly across the three groups. The Lethary and Stereotypy subscales of the ABC were highly significant (P < 0.001) in distinguishing the three groups from one another. Within the ASD group differences were apparent by DSM-IV type on the Lethargy subscale, which reached significance, ANOVA (F = 0.002) and t-test (Autism > PDD, P = 0.005; PDD < CDD, P = 0.002). Using a multivariate regression model, the ABC scales alone explained 62% of variance of ASD outcome; addition of demographic variables explained up to 68% of the variance. There is good correlation between DSM-IV criteria for autism and subscales scores on the ABC in subjects with DS. This study demonstrates the feasibility of using the ABC to characterize the neurobehavioral phenotype of a cohort of children with trisomy 21 and ASD for ongoing research purposes.
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PMID:Down syndrome and comorbid autism-spectrum disorder: characterization using the aberrant behavior checklist. 1575 62

Polychlorinated biphenyls (PCBs) and hydroxy-PCB (OH-PCB) metabolites are widely distributed bioaccumulative environmental chemicals and have similar chemical structures to those of thyroid hormones (THs). Previously, we reported that THs are essential for neuronal development and the low doses of two OH-PCBs, namely, 4-OH-2',3,3',4',5'-pentachlorobiphenyl (4'-OH-PeCB-106) and 4-OH-2',3,3',4',5,5'-hexachlorobiphenyl (4'-OH-HxCB-159), inhibited the TH-dependent dendritic development of Purkinje cells in mouse cerebellar cultures using serum-free defined medium. To determine which type of OH-PCBs affect neuronal development, we further examined several OH-PCBs and other estrogenic chemicals using this simple and sensitive assay system. Two-way ANOVA was used to assess the effects of OH-PCBs and other chemicals on both factors of their concentrations and with/without T4 in the assay of TH-dependent dendritic development of Purkinje cells. Aside from the two OH-PCBs, 4-OH-2',3,4',5,6'-pentachlorobiphenyl (4'-OH-PeCB-121) and bisphenol A significantly inhibited the TH-dependent dendritic development of Purkinje cells, whereas 4-OH-2',3,3',5',6'-pentachlorobiphenyl (4'-OH-PeCB-112), 4-OH-2',3,3',5,5',6'-hexachlorobiphenyl (4'-OH-HxCB-165), 4-OH-2,2',3,4',5,5',6-heptachlorobiphenyl (4-OH-HpCB-187), progesterone and nonylphenol did not induce any inhibition, but significantly promoted the dendritic extension of Purkinje cells in the absence of THs. Other estrogenic chemicals, including beta-estradiol, diethyl stilbestrol and p-octylphenol did not show significant inhibitory or promoting effects. From these results, it is suggested that exposure to OH-PCBs and other environmental chemicals may disrupt normal neuronal development and cause some developmental brain disorders, such as LD, ADHD, and autism.
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PMID:Disrupting effects of hydroxy-polychlorinated biphenyl (PCB) congeners on neuronal development of cerebellar Purkinje cells: a possible causal factor for developmental brain disorders? 1722 78

It is unknown whether the Autism-spectrum quotient (AQ) can discriminate between Autism Spectrum Disorder (ASD) and Attention Deficit and Hyperactivity Disorder (ADHD) with or without comorbid Substance Use Disorder (SUD). ANOVA's were used to analyse the mean AQ (sub)scores of 129 adults with ASD or ADHD. We applied receiver operating characteristic (ROC) computations to assess discriminant power. All but one of the mean AQ (sub)scores were significantly higher for adults with ASD compared to those with ADHD. The SUD status in general was not significantly associated with AQ (sub)scores. On the Social Skills subscale patients with ASD and comorbid SUD showed less impairment than those without SUD. The cut-off score 26 yielded 73% correct classifications. The clinical use of the AQ in differentiating between ASD and ADHD is limited.
J Autism Dev Disord 2009 Sep
PMID:Using the Autism-spectrum quotient to discriminate Autism Spectrum Disorder from ADHD in adult patients with and without comorbid Substance Use Disorder. 1939 35


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