Alterations in Plasma Cytokine Levels in Korean Children with Autism Spectrum Disorder.

Purpose: Numerous studies have supported the role of the immune dysfunction in the pathogenesis of autism spectrum disorder (ASD); however, to our knowledge, no study has been conducted on plasma cytokine levels in children with ASD in South Korea. In this study, we aimed to analyze the immunological characteristics of Korean children with ASD through plasma cytokine analysis.

Materials And Methods: Blood samples were collected from 94 ASD children (mean age 7.

Association between autism spectrum disorder and inflammatory bowel disease: A systematic review and meta-analysis.

Children with autism spectrum disorder (ASD) are frequently diagnosed with co-occurring medical conditions including inflammatory bowel disease (IBD). To investigate the association, we conducted a systematic review registered in PROSPERO (ID:CRD42021236263) with a random-effects meta-analysis. We searched PubMed, Embase, and PsycInfo (last search on January 25, 2021), and manually searched relevant publications.

Pilot study of a mobile application-based intervention to induce changes in neural activity in the frontal region and behaviors in children with attention deficit hyperactivity disorder and/or intellectual disability.

Children with neurodevelopmental disorders, such as attention deficit hyperactivity disorder (ADHD) and intellectual disability (ID), need early intervention and continuous treatment. We aimed to investigate the feasibility and acceptability of mobile application-based interventions in children with ADHD and ID in supporting attention and cognitive function. Twenty-six children with ADHD and/or ID with attention and cognition difficulties were recruited.

The Role of Ion Channel-Related Genes in Autism Spectrum Disorder: A Study Using Next-Generation Sequencing.

The clinical heterogeneity of autism spectrum disorder (ASD) is closely associated with the diversity of genes related to ASD pathogenesis. With their low effect size, it has been hard to define the role of common variants of genes in ASD phenotype. In this study, we reviewed genetic results and clinical scores widely used for ASD diagnosis to investigate the role of genes in ASD phenotype considering their functions in molecular pathways.

Altered Gut Microbiota in Korean Children with Autism Spectrum Disorders.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by social and behavioral impairments. Recent studies have suggested that gut microbiota play a critical role in ASD pathogenesis. Herein, we investigated the fecal microflora of Korean ASD children to determine gut microbiota profiles associated with ASD.

Differences in Language Ability and Emotional-Behavioral Problems according to Symptom Severity in Children with Autism Spectrum Disorder.

Purpose: The aim of this study was to investigate differences in language ability and emotional-behavioral problems according to the severity of social communication impairments (SCI) and restricted and repetitive behaviors (RRB) in children with autism spectrum disorders (ASD).

Materials And Methods: We grouped 113 children with ASD aged 3-12 years according to the severity of SCI and RRB, and investigated language differences and emotional-behavioral problems among the severity groups. If differences in language abilities between the groups were observed, they were further subdivided to examine possible predictors of both receptive and expressive language abilities.

Effects of a Dehydroevodiamine-Derivative on Synaptic Destabilization and Memory Impairment in the 5xFAD, Alzheimer's Disease Mouse Model.

Carboxy-dehydroevodiamine·HCl (cx-DHED) is a derivative of DHED, which improves memory impairment. Carboxyl modification increases solubility in water, indicating that its bioavailability is higher than that of DHED. Cx-DHED is expected to have better therapeutic effects on Alzheimer's disease (AD) than DHED.

Aberrant Neural Activation Underlying Idiom Comprehension in Korean Children with High Functioning Autism Spectrum Disorder.

Purpose: Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by social communication impairments and repetitive behaviors or restricted interests. Impaired pragmatic language comprehension is a universal feature in individuals with ASD. However, the underlying neural basis of pragmatic language is poorly understood.

Human adipose-derived stem cells ameliorate repetitive behavior, social deficit and anxiety in a VPA-induced autism mouse model.

Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by impairments in social interaction and communication, and patients often display co-occurring repetitive behaviors. Although the global prevalence of ASD has increased over time, the etiology and treatments for ASD are poorly understood. Recently, some researchers have suggested that stem cells have therapeutic potential for ASD.

Dehydroevodiamine•HCl Protects Against Memory Impairment and Cerebral Amyloid-β Production in Tg2576 Mice by Acting as a β-Secretase Inhibitor.

We previously demonstrated that dehydroevodiamine•HCl (DHED), which was purified from Evodia rutaecarpa Bentham (Rutaceae), has beneficial effects on memory impairment and neuronal damage in three disease models. To investigate the preventive action of DHED in Alzheimer's disease (AD), a progressive neurodegenerative disorder characterized by memory decline, amyloid-β (Aβ) protein-containing neuritic plaques and neurofibrillary tangles, in this study, we proposed that DHED may be therapeutically effective against the memory impairment and disease-related neurochemical changes that occur in Tg2576 (Tg) mice. DHED (0.

Characteristics of Brains in Autism Spectrum Disorder: Structure, Function and Connectivity across the Lifespan.

Autism spectrum disorder (ASD) is a highly prevalent neurodevelopmental disorder characterized by impaired social communication and restricted and repetitive behaviors (RRBs). Over the past decade, neuroimaging studies have provided considerable insights underlying neurobiological mechanisms of ASD. In this review, we introduce recent findings from brain imaging studies to characterize the brains of ASD across the human lifespan.

S100A9 knockout decreases the memory impairment and neuropathology in crossbreed mice of Tg2576 and S100A9 knockout mice model.

Our previous study presented evidence that the inflammation-related S100A9 gene is significantly upregulated in the brains of Alzheimer's disease (AD) animal models and human AD patients. In addition, experiments have shown that knockdown of S100A9 expression improves cognition function in AD model mice (Tg2576), and these animals exhibit reduced amyloid plaque burden. In this study, we established a new transgenic animal model of AD by crossbreeding the Tg2576 mouse with the S100A9 knockout (KO) mouse.

In vivo imaging of human adipose-derived stem cells in Alzheimer's disease animal model.

Stem cell therapy is a promising tool for the treatment of diverse conditions, including neurodegenerative diseases such as Alzheimer's disease (AD). To understand transplanted stem cell biology, in vivo imaging is necessary. Nanomaterial has great potential for in vivo imaging and several noninvasive methods are used, such as magnetic resonance imaging, positron emission tomography, fluorescence imaging (FI) and near-infrared FI.

The therapeutic effects of human adipose-derived stem cells in Alzheimer's disease mouse models.

Alzheimer's disease (AD) is an irreversible neurodegenerative disease, still lacking proper clinical treatment. Therefore, many researchers have focused on the possibility of therapeutic use of stem cells for AD. Adipose-derived stem cells (ASCs), mesenchymal stem cells (MSCs) isolated from adipose tissue, are well known for their pluripotency and their ability to differentiate into multiple tissue types and have immune modulatory properties similar to those of MSCs from other origins.

Amyloid precursor protein binding protein-1 knockdown reduces neuronal differentiation in fetal neural stem cells.

Amyloid precursor protein binding protein-1 (APP-BP1) was first identified as an interacting protein of APP. In this study, we explored whether APP-BP1 plays a role in neuronal differentiation of fetal neural stem cells. APP-BP1 knockdown by small interfering RNA treatment was found to downregulate neuronal differentiation and to upregulate APP intracellular domain production from APP in fetal neural stem cells.

Focal transient ischemia increases APP-BP1 expression in neural progenitor cells.

Amyloid precursor protein binding protein-1 (APP-BP1) binds to the carboxyl terminus of APP. In this study, we explored whether APP-BP1 expression is affected by focal transient cerebral ischemia induced by middle cerebral artery occlusion in Wistar rats. APP-BP1 expression was increased in the dentate gyrus of the hippocampus and in the subventricular zone of rats exposed to focal transient cerebral ischemia.

Amyloid precursor protein binding protein-1 modulates cell cycle progression in fetal neural stem cells.

Amyloid precursor protein binding protein-1 (APP-BP1) binds to the carboxyl terminus of the amyloid precursor protein (APP) and serves as the bipartite activation enzyme for the ubiquitin-like protein, NEDD8. In the present study, we explored the physiological role of APP-BP1 in the cell cycle progression of fetal neural stem cells. Our results show that cell cycle progression of the cells is arrested at the G1 phase by depletion of APP-BP1, which results in a marked decrease in the proliferation of the cells.

Amyloid Precursor Protein Binding Protein-1 Is Up-regulated in Brains of Tg2576 Mice.

Amyloid precursor protein binding protein-1 (APP-BP1) binds to the carboxyl terminus of amyloid precursor protein and serves as a bipartite activation enzyme for the ubiquitin-like protein, NEDD8. Previously, it has been reported that APP-BP1 rescues the cell cycle S-M checkpoint defect in Ts41 hamster cells, that this rescue is dependent on the interaction of APP-BP1 with hUba3. The exogenous expression of APP-BP1 in neurons has been reported to cause DNA synthesis and apoptosis via a signaling pathway that is dependent on APP-BP1 binding to APP.