Scale of Emotional Development - Short: reliability and validity in adults with intellectual disability.

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.

[Adults with Intellectual Disability and Mental Disorder Respectively Challenging Behaviour: System-Related Strategies for Coping with Aggressive Incidents].

A large interview study, evolved from the clinical research project SYMPA-ID (Systemic Methods in Acute Psychiatry for People with Intellectual Disability), focused on adults with cognitive impairment and mental disorder who lived in a residential home and were in need of intensive psychiatric treatment. With the objective of analysing the interactions between the patients and their carers as well as the cooperations within the multi-carer system, both patients with mild to severe ID and their carers (relatives, legal guardians, professional carers of residential group homes as well as in- and outpatient psychiatric services) were surveyed several times between 2015 and 2018. Qualitative Data Analysis of 188 interviews with 67 participants resulted in a collection of 43 strategies concerning both attitudes and activities to prevent or cope with aggressive incidents.

[Pilot study of psychiatric and social aspects of children and adolescents with fragile X syndrome].

Objective: The study describes the burden of psychosocial risks of mental illnesses and the ways in which children and adolescents with fragile X syndrome (FRX) can be treated.

Method: Data from a sample of 34 patients with FRX younger than 18 years stemming from a prospective multicenter (n = 11) registry study (EXPLAIN) were analyzed with regard to psychosocial burden and Treatment.

Results: One third of all participants reported having relatives who suffer from FRX.

Characterization, treatment patterns, and patient-related outcomes of patients with Fragile X syndrome in Germany: final results of the observational EXPLAIN-FXS study.

Background: As data on the phenotype, characteristics and management of patients with Fragile X Syndrome (FXS) are limited, we aimed to collect such data in Germany in experienced centres involved in the treatment of such patients.

Methods: EXPLAIN-FXS is a prospective observational (non-interventional) study (registry) performed between April 2013 and January 2016 at 18 sites in Germany. Requirements for patient participation included confirmed diagnosis of FXS by genetic testing (>200 CGG repeats) and written informed consent.

[Psychiatric and Social Aspects of Patients with Fragile X Syndrome].

Objective: The goal of the study was to describe the burden of psychosocial risks, of mental illnesses and the ways of treatment of patients with fragile X syndrome (FRX).

Method: Data from a sample of 46 FRX-patients stemming from a prospective multicenter (N = 12) registry study (EXPLAIN) were analyzed with regard to psychosocial burden and treatment.

Results: More than 50 % of all participants reported about relatives suffering from FRX, too.

EXPLAIN Fragile-X: an explorative, longitudinal study on the characterization, treatment pathways, and patient-related outcomes of Fragile X Syndrome.

Background: Fragile X syndrome (FXS), caused by a mutation of the FMR1 gene on the X chromosome, is the most common inherited form of intellectual disability and autism spectrum disorders. Comprehensive data are lacking, however, on the characteristics and management patients with FXS in Germany.

Methods/design: EXPLAIN is a prospective, observational, longitudinal registry with a non-probability sampling approach.

Sensory ganglia require neurotrophin-3 early in development.

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.

A crucial role for neurotrophin-3 in oligodendrocyte development.

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.