View clinical trials related to Autistic Disorder.
Filter by:This study aims to compare two screening strategies for identifying infants with a potential risk of Autism Spectrum and Neurodevelopmental Disorders to provide early access to care and increase the likelihood of a favorable outcome
Autism spectrum disorder (ASD) is a neurodevelopmental disorder of unclear etiology. There are theories depicting the importance of sex steroid hormones in autism, since the prevalence of the disorder is male-biased. What makes boys more vulnerable to achieve the diagnosis of autism remains unclear. One of the theories strengthens the importance of fetal organizational effect of testosterone on brain development. Baron Cohen with coworkers showed that elevated fetal levels of several androgens including testosterone were high in male-fetuses who later in postnatal life achieved the diagnosis of autism and fetal testosterone levels were positively correlated with autistic traits in general population. Females with conditions of abnormal prenatal exposure to testosterone and its sex steroid precursors, such as congenital adrenal hyperplasia and polycystic ovary syndrome, were found to have higher rate of autistic traits as well as their children were of higher risk of developing autism. However, the exact mechanism by which these hormones influence the manifestation of autistic traits remains undiscovered. Another model explaining higher prevalence of ASD in males is a female protective model which suggests that multiple genetic factors contribute to the development of ASD and that higher threshold of genetic liability is required in females compared to males. Zhang et al. demonstrated genetic evidence of sex differences in ASD confirming female protective model, employing investigation of de novo mutations, common variants of ASD candidate genes and their co-expression in male and female brain. During infancy: The Gonadotropin releasing hormone (GnRH) pulse generator is reactivated by 6 to 10 days after birth. This period, termed the mini puberty of infancy, was first described in the 1970s. During mini puberty, luteinizing hormone (LH) levels approximate pubertal concentrations, reaching a peak between 16 and 20 days of life. Serum testosterone levels rise in response to rising concentrations of LH, paralleling an increase in Leydig cell number and testicular testosterone concentrations. Serum testosterone levels peak from 1 to 3 months (210 ± 130 ng/dL or 7.28 ± 4.51 nmol/L on day of life 30) and decline by roughly 50% per month reaching prepubertal levels by 7 to 12 months of age. Dihydrotestosterone (DHT) concentrations parallel the rise in testosterone, reaching pubertal values during the early postnatal period. During puberty: Testosterone is produced primarily by the testes, though a small amount is also made in the adrenal gland. Gonadarche refers to the onset of sex steroid production from the gonads and occurs in response to pulsatile production of GnRH from the hypothalamus, which in turn stimulates production of LH and Follicle stimulating hormone (FSH) from the pituitary gland. LH stimulates the Leydig cells to produce testosterone, whereas FSH stimulates the Sertoli cells to proliferate and initiate spermatogenesis. Active androgens are synthesized via two alternative pathways. The first of them is known as the classic "frontdoor" pathway with pregnenolone serving as androgen precursor, which underwent a conversion to DHEA and subsequently to androstenediol. These metabolic steps are catalyzed by CYP17A1 (in the C17,20-lyase step) and (mostly adrenal) AKR1C3 enzyme, respectively. Dehydroepiandrosterone (DHEA) and androstenediol are readily sulfated by SULT2A1 in adrenal cortex and their sulfates serve as the stock pool for the production of active androgens of the adrenal origin as the production of androgens in early childhood of boys is limited to extra-gonadal tissues, such as adrenal, skin, etc. These sulfated primary androgens may be subsequently deconjugated and metabolized by HSD3B1 and HSD3B2 isoforms to androstenedione and Total testosterone (TST) and then to 5α/β-reduced 17-oxo- and 17β-androgens, respectively. In addition, the androstenedione may be readily converted to testosterone by adrenal AKR1C3. From the aforementioned substances, TST, 5α-dihydrotestosterone, and 11-oxo-testosterone are known as the most potent bioactive androgens. Besides the "frontdoor" pathway the dihydrotestosterone may be also formed by so called "backdoor" pathway. This pathway is based on a direct conversion of 5α/β-reduced pregnane steroids (C21) to their 5α/β-reduced androgen (C19) metabolites which is catalyzed by the same enzyme converting pregnenolone to DHEA (CYP17A1 in the C17,20-lyase step). These 5α/β-reduced androgen (C19) metabolites include also the most active androgen 5α-dihydrotestosterone. The "backdoor" pathway is crucial for androgen synthesis in marsupials but may also be active in various human steroid-related disorders.
Evaluate some Inflammatory markers [IL-6, IL-8, TNF_alpha] in children with autism spectrum disorder
In the present study, we aim to evaluate the serum level of 25 hydrxy vitamin D in autistic children .
To reach a feasible method for diagnosing Autism Spectrum Disorder (ASD) outcome measures: 1. Primary (main): Measurement of various brain structures, including the total brain volume, the volumes of specific brain regions (such as the amygdala, hippocampus, and cerebellum), and the thickness of the cortex. Detection of other concurrent lesions, e.g. tuberous sclerosis 2. Secondary (subsidiary): levels of various neurotransmitters, such as glutamate and GABA, and other metabolites, such as N-acetyl aspartate (NAA), in specific regions of the brain Assessing neural activity and connectivity in the brain in the resting state
This is an 18 to 54 week study assessing the efficacy of Full-Spectrum Medicinal Cannabis Plant Extract 0.08% THC (NTI164) on the severity of autism spectrum disorder in young people.
The goal of this prospective observational multicentric cohort study is to evaluate the clinical prognostic value of the speech tracking score of language development in children with ASD aged from 3 years to 4 years and half at inclusion. Participants will followed during 4 years with an annual visit. During these visits, each participant will be clinically evaluated (scales and tests) and performed an EEG-HR recording. Two groups will be formed, one with children diagnosed with ASD with language delay, and a control group composed of non-ASD children without language delay, matched on age and gender with the ASD group.
The purpose of the LIFT study is to develop a technology-assisted adaptation of the JASPER (Joint Attention, Symbolic Play, Engagement, and Regulation: Kasari et al., 2021) social communication intervention for young children with autism spectrum disorder (ASD). In partnership with community early intervention (EI) and early childhood special education (ECSE) practitioners in Oregon, implementation strategies to help caregivers learn to the use the intervention strategies with their young children will delivered in a pilot randomized trial. The pilot trial will compare primarily self-directed learning through online materials and brief practitioner support (ONLINE) with the addition of live synchronous coaching (ONLINE + COACH) on caregivers' strategy use (primary) and children's joint engagement and social communication (secondary).
In this study, a selective and multi-stages screening for neurodevelopmental disorders (NDD) in siblings of children with a confirmed ASD is done. The main aims are to estimate the prevalence of NDD among siblings and to evaluate the feasibility and acceptability of a standardized screening procedure.
Children with Autism spectrum disorders have speech disorders, which in turn aggravate communication difficulties and lead to an increase in their core symptoms. This experiment attempts to investigate the efficacy of Chinese language oral motor therapy in improving various aspects of articulation, language ability, and behavior of children with autism in conjunction with the International General Autism Scale, and provides a basis for the rational formulation of clinical treatment plans.