ASD-associated mutations induced changes in the localization of α-actinin-4, which localized less to dendritic spines, and for SWAP-70 and SrGAP3, which localized more to dendritic spines.
This study was designed to (1) describe ASD symptoms in adolescent and young adult males with FXS (n = 44) and (2) evaluate the contributions to ASD severity of cognitive, language, and psychiatric factors, as well as FMRP (the protein deficient in FXS).
At the group-level, we observed weaknesses in the language skills of boys with <sub>n</sub>ASD relative to those with FXS (e.g., when considering raw score performance, standard score performance relative to nonverbal cognitive skills, frequency of talk in play), after controlling for nonverbal IQ and ASD symptom severity.
The research put forward that in individuals with ASD, while gluten-free/casein-free and ketogenic diets, camel milk, curcumin, probiotics, and fermentable foods can play a role in alleviating ASD symptoms, consumption of sugar, additives, pesticides, genetically modified organisms, inorganic processed foods, and hard-to-digest starches may aggravate symptoms.
In view of the high prevalence of familial occurrence of secundum ASD (10% of all ASD patients), we recommend screening all first degree relatives of ASD patients for cardiac, conduction and skeletal anomalies.
To investigate possible correlates of generalised anxiety disorder (GAD) in young males with ASD, a test of the mediation effects of sensory features (SF) upon the association between ASD symptoms and GAD was conducted with 150 males aged 6 to 18 years.
We aimed to develop and internally validate a scoring system, the adult spinal deformity surgical decision-making (ASD-SDM) score, to guide the decision-making process for ASD patients aged above 40 years.
Heart rate variability (HRV) has been separately shown to be associated with ASD symptomatology, psychological wellbeing and emotion regulation (ER) in specific samples consisting of either individuals with ASD, those without ASD, or combined.
Asparagine Synthetase Deficiency (ASD) is a recently described inborn error of metabolism caused by bi-allelic pathogenic variants in the asparagine synthetase (ASNS) gene.
ASD significantly increased the expression of anti-oxidant enzymes (GSH, SOD, and CAT) in both liver and vascular tissue, reduced blood lipid levels (TG, TC, and LDL-C), and decreased lipid deposition in the liver and atherosclerotic lesion size in ApoE<sup>-/-</sup> mice.