ABSTRACT
BACKGROUND: Intellectual disability (ID) is often associated with delays in emotional development (ED). The Scale of Emotional Development - Short (SED-S) was developed to assess the level of ED and to adapt treatment and care accordingly. METHODS: In a sample of 724 adults from five study sites in three countries, a confirmatory factor analysis with a one-factor model was conducted on the entire dataset as well as in different subgroups. Furthermore, internal consistency was investigated using Cronbach's alpha. RESULTS: The confirmatory factor analysis indicated that a single-factor model fits the SED-S data well. The subgroup analyses revealed good model fit, regardless of the severity of ID and irrespective of sex or the presence of autism spectrum disorder or psychiatric disorders. Internal consistency was excellent for the entire sample (Cronbach's alpha = 0.93) and various subgroups (0.869-0.938). CONCLUSION: The results of this study suggest that the SED-S is psychometrically sound and can be used to assess the level of ED in adults with ID.
Subject(s)
Autism Spectrum Disorder , Intellectual Disability , Humans , Adult , Autism Spectrum Disorder/diagnosis , Reproducibility of Results , Emotions , Factor Analysis, Statistical , SeizuresABSTRACT
The role played by neurotrophin-3 during the development of quail sensory ganglia was investigated using a monoclonal antibody that specifically blocks the biological activity of this neurotrophin. Neutralisation of neurotrophin-3 was initiated during completion of gangliogenesis. Neuronal cell counts indicate that about 30% of the neurons normally present in either the placode-derived ganglion nodosum or in a leg-innervating, neural crest-derived dorsal root ganglion are eliminated by the antibody treatment. In both ganglia, this reduction is seen early in development, and the results obtained with the ganglion nodosum indicate that neurotrophin-3 plays an essential role already during gangliogenesis. Neuronal numbers are also compared with those obtained after treatment with a monoclonal antibody to nerve growth factor, used either alone or in combination with the neurotrophin-3 antibody.
Subject(s)
Ganglia, Sensory/embryology , Nerve Growth Factors/physiology , Quail/embryology , Animals , Antibodies, Monoclonal , Cell Count , Ganglia, Sensory/cytology , Mice , Mice, Inbred BALB C , Morphogenesis/physiology , Nerve Growth Factors/immunology , Neurons/cytology , Neurotrophin 3ABSTRACT
The neurotrophins nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3 and neurotrophin-4/5 promote the survival of subpopulations of vertebrate neurons in vitro, but so far only nerve growth factor has been demonstrated to be essential for normal neuronal development; no neurotrophin has previously been shown to function in normal glial cell development. We found recently that neurotrophin-3 promotes the survival of pure oligodendrocyte precursor cells in vitro, and, although by itself it induces only a small percentage of these cells to synthesize DNA, in combination with platelet-derived growth factor it induces the majority of them to do so. Neither of these factors, however, has been shown to contribute to oligodendrocyte precursor cell proliferation in vivo or to stimulate pure populations of these cells to proliferate (as opposed to synthesize DNA) in vitro. Here we show that neurotrophin-3 and platelet-derived growth factor collaborate to promote clonal expansion of oligodendrocyte precursor cells in vitro and to drive the intrinsic clock that times oligodendrocyte development. We also show that neurotrophin-3 helps stimulate the proliferation of oligodendrocyte precursor cells in vivo and is thus required for normal oligodendrocyte development.
