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Query: UMLS:C0025362 (mental retardation)
 15,878 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to compare the periodontal condition of children with Down's syndrome and other types of mental retardation with normal children. We used two indexes: a plaque index and a gingival index. By means of the student t-test and ANOVA statistical procedure, we found the following. Mentally retarded children had a higher average intelligence than children with Down's syndrome, and significant differences existed among the three groups on both the plaque index and the gingival index, while sex had no influence on these results.
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PMID:[Survey on oral hygiene status in children with Down's syndrome and mental retardation]. 184 Mar 20

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

Prader-Willi syndrome (PWS) is a genetic disorder occurring in 1 of 10,000-16,000 live births and is characterized by excessive appetite with progressive massive obesity as well as short stature and mental retardation. Most patients have GH deficiency and hypogonadotropic hypogonadism. The causes of the hyperphagia and abnormal GH secretion are unknown. To determine whether ghrelin, a novel GH secretagogue with orexigenic properties, is elevated in PWS, we measured fasting plasma ghrelin concentration; body composition (dual-energy x-ray absorptiometry); and subjective ratings of hunger (visual analog scale) in seven subjects (6 males and 1 female; age, 26 +/- 7 yr; body fat, 39 +/- 11%, mean +/- SD) with PWS (diagnosis confirmed by genetic test) and 30 healthy subjects (reference population, 15 males and 15 females; age, 32 +/- 7 yr; body fat, 36 +/- 11%) fasted overnight. All subjects were weight stable for at least 6 months before admission to the study. The mean plasma ghrelin concentration was higher in PWS than in the reference population (307 +/- 164 vs. 109 +/- 24 fmol/ml; P < 0.001), and this difference remained significant after adjustment for percentage body fat (P < 0.001). Plasma ghrelin was also higher (P = 0.0004) in PWS than in five healthy subjects fasted for 36 h. A positive correlation was found between plasma ghrelin and subjective ratings of hunger (r = 0.71; P = 0.008). Furthermore, in subjects with PWS, the concentration of the hormone was not different before and after ingestion of 2 ml and a satiating amount of the same liquid meal (ghrelin concentrations: 307 +/- 164 vs. 306 +/- 205 vs. 260 +/- 134 fmol/ml, respectively; ANOVA for repeated measures, P = 0.56). This is the first evidence that ghrelin, a novel orexigenic hormone, is elevated in subjects with PWS. Our finding suggests that ghrelin may be responsible, at least in part, for the hyperphagia observed in PWS.
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PMID:High circulating ghrelin: a potential cause for hyperphagia and obesity in prader-willi syndrome. 1246 37

To understand the commitment of the genome to nervous system differentiation and function, we sought to compare nervous system gene expression to that of a wide variety of other tissues by gene expression database construction and mining. Gene expression profiles of 10 different adult nervous tissues were compared with that of 72 other tissues. Using ANOVA, we identified 1,361 genes whose expression was higher in the nervous system than other organs and, separately, 600 genes whose expression was at least threefold higher in one or more regions of the nervous system compared with their median expression across all organs. Of the 600 genes, 381 overlapped with the 1,361-gene list. Limited in situ gene expression analysis confirmed that identified genes did represent nervous system-enriched gene expression, and we therefore sought to evaluate the validity and significance of these top-ranked nervous system genes using known gene literature and gene ontology categorization criteria. Diverse functional categories were present in the 381 genes, including genes involved in intracellular signaling, cytoskeleton structure and function, enzymes, RNA metabolism and transcription, membrane proteins, as well as cell differentiation, death, proliferation, and division. We searched existing public sites and identified 110 known genes related to mental retardation, neurological disease, and neurodegeneration. Twenty-one of the 381 genes were within the 110-gene list, compared with a random expectation of 5. This suggests that the 381 genes provide a candidate set for further analyses in neurological and psychiatric disease studies and that as a field, we are as yet, far from a large-scale understanding of the genes that are critical for nervous system structure and function. Together, our data indicate the power of profiling an individual biologic system in a multisystem context to gain insight into the genomic basis of its structure and function.
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PMID:Neural system-enriched gene expression: relationship to biological pathways and neurological diseases. 1512 45

The walking activity of men and women with mental retardation residing in community settings was described. Participants were 38 women (M age=.7, SD=9.5) and 65 men (M age=35.9, SD=11.2). They wore pedometers for 7 days. A 2 x 2 factorial ANOVA indicated no significant gender differences in total step counts or between participants with and those without Down syndrome. A post-hoc analysis revealed that participants walked less on Saturday than during the weekdays. Only 21.1% of the women and 21.5% of the men with mental retardation accumulated the recommended 10,000 steps per day.
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PMID:Walking habits of adults with mental retardation. 1626 10

Fragile X syndrome (FXS) is the most common form of inherited mental retardation (MR). FXS is typically caused by a mutation of the Fmr1 gene (Verkerk et al. 1991, Cell 65, 905-914). To better understand the role of Fmr1 and its gene product fragile X mental-retardation protein (FMRP) in central nervous system function, researchers have turned to the use of animal model systems to generate an Fmr1 knockout (KO) mouse that is deficient in FMRP (Bakker et al. 1994, Cell 78, 23-33). Unfortunately, a number of studies have found no consistent, robust learning and memory impairment in the Fmr1 KO mice. We conducted a study to assess the performance of Fmr1 KO and wildtype (WT) animals in a leverpress escape/avoidance paradigm. Fmr1 KO and WT littermates were studied in four daily 1-h sessions. The Fmr1 KO mice performed fewer avoidance and total responses than WT mice. The KO animals were not simply deficient in avoidance, but a within-factor ANOVA revealed that they did not acquire the leverpress response to any appreciable degree. Observation during the sessions indicated that the Fmr1 KO animals clearly responded to the shock, eliminating an obvious sensory explanation for the deficit. The fact that other studies have found that the KO mice displayed increased exploratory and locomotor activity compared with WT controls argues against a motoric deficit. Future studies will attempt to delineate the nature of the behavioral deficit as well as attempt to rescue the response with glutamatergic or dopaminergic agents.
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PMID:Fmr1 knockout mice are impaired in a leverpress escape/avoidance task. 1692 51

Advanced parental age has been shown to increase offspring risk for a number of neuropsychiatric disorders including schizophrenia and Down's syndrome. Other psychiatric disorders have been less studied with respect to the effect of parental age on offspring risk. In this study we examine if advanced parental age increased risk for ICD-10 diagnoses. We hypothesized that advanced parental age would increase risk for offspring psychotic disorders and mental retardation but not other ICD-10 diagnoses. We examined follow-up data for 30,965 subjects treated in outpatient psychiatric facilities between 1980 and 2007. Subjects were younger than 18 years of age at their first outpatient visit. A comparison group was obtained from data on registered births in Spain from 1975. We compared parental age (maternal, paternal, combined) across diagnostic categories using ANOVA and logistic regression was used to estimate the risk of psychopathology in the offspring with advanced parental age (maternal, paternal, combined). Maternal and paternal ages were higher for subjects diagnosed with mental retardation. Risk for psychotic disorders showed a significant linear increase only with advancing maternal age, and not paternal age as is more often reported.
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PMID:Differences in maternal and paternal age between schizophrenia and other psychiatric disorders. 1994 57

The purpose of this study was to investigate the effects of physical training and calcium intake on bone mineral density (BMD) of students with mental retardation. Forty mentally retarded boys (age 7-10 years old) were randomly assigned to four groups (no differences in age, BMD, calcium intake and physical activity): training groups with or without calcium supplementation (Tr+Ca+ and Tr+Ca-) and nontraining groups with or without calcium supplementation (Tr-Ca+ and Tr-Ca-). The intervention involved 45 min of physical training performed 3 sessions a week and/or the addition of dietary calcium-rich food using enriched cow milk with vitamin D containing 230 mg calcium per serving, over 6 months. Paired-samples t-test and ANOVA analysis was used to determine the main and combined effects of training and calcium on BMD. All groups showed greater femoral neck BMD after 6 months. The increase in femoral neck BMD in the Tr+Ca+ group was 10% greater than increase in the Tr+Ca- group (not significant). Apparently, the effect of training was greater than calcium intake because the Tr+Ca- group achieved 4% greater BMD than Tr-Ca+ group (not significant). In this study, both training groups had greater BMD than the control group (Tr-Ca-) (P<0.05). In these participants with inadequate calcium intakes, additional exercise and calcium supplementation resulted in a 6-20% greater increase in BMD than controls at the loaded site (femoral neck). These results help to provide more evidence for public health organizations to deal with both exercise and nutrition issues in children for the achievement of peak BMD.
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PMID:Effects of physical training and calcium intake on bone mineral density of students with mental retardation. 2029 86

The purpose of this study was to assess the respiratory muscle strength (RMS) in individuals with mental retardation (MR), with or without Down Syndrome (DS), and its association with bone mineral density (BMD). Forty-five male individuals (15 with DS, 15 with mental retardation (MR) and 15 apparently healthy controls), aged 20-35, participated in this study. Subject assessment included pulmonary function tests, RMS (maximal inspiratory pressure, MIP, and maximal expiratory pressure, MEP) and BMD of the second and fourth lumbar vertebrae. ANOVA was used to test differences amongst groups. Tukey post hoc test was utilized when significant differences were detected with ANOVA. Bivariate correlation for BMD and respiratory muscle strength was calculated with Pearson's coefficient of correlation. Individuals with MR, both with and without DS, have lower FEV1, FVC, MIP and MEP (p<0.001) compared to controls. Individuals with DS also had lower BMD, which was associated with lower MIP and MEP. Hypotonia, sedentary lifestyle and obesity are factors that may explain lower MIP and MEP in DS. Strategies to increase RMS could decrease the risk of osteoporosis in the DS population.
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PMID:Bone mineral density and respiratory muscle strength in male individuals with mental retardation (with and without Down Syndrome). 2054 8


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