scholarly journals ESSENTIAL ELEMENTS IN THE ETIOLOGY AND PATHOGENESIS OF AUTISM SPECTRUM DISORDER IN CHILDREN

2020 ◽  
Vol 21 (4) ◽  
pp. 32-39
Author(s):  
L.N. Chernova ◽  
Keyword(s):  
Oxidative Stress ◽  
Autism Spectrum Disorder ◽  
Central Nervous System ◽  
Nervous System ◽  
Autism Spectrum ◽  
Essential Elements ◽  
Nerve Fibers ◽  
Spectrum Disorder ◽  
Epileptiform Discharges ◽  
Antioxidant Defense Systems

A large number of studies have been conducted up to date associated with the elemental status of children with Autism Spectrum Disorder (ASD). However, it is still difficult to fully explain the relationship between ASD and elements due to previous inconsistent scientific results. The article reviews the possible role of essential elements in the etiopathogenesis of ASD in children. An imbalance of essential elements can cause a disruption in development of central nervous system. It leads to impaired differentiation and proliferation of neurons and disruption in myelination, affects neurochemistry and neurotransmitter balance, provokes oxidative stress and neuroinflammation. In particular, the balance of trace elements such as copper, iron and selenium is necessary to maintain the antioxidant defense systems. Increased levels of free radicals lead to cellular damage, oxidative stress and neuroinflammation linked to ASD. Magnesium and calcium, acting as secondary messengers in the central nervous system (CNS), regulate the processes of neural networks’ maturation and neurotransmitter release. An imbalance of potassium and sodium changes electrical activity of the brain and may be the cause of epileptiform discharges in ASD. Zinc provides the processes of neuronal migration and neurotransmission, while copper, iodine and iron contribute to myelination of nerve fibers.

scholarly journals Update on Atypicalities of Central Nervous System in Autism Spectrum Disorder

2020 ◽  
Vol 10 (5) ◽  
pp. 309
Author(s):  
Ahmad Naqib Shuid ◽  
Putri Ayu Jayusman ◽  
Nazrun Shuid ◽  
Juriza Ismail ◽  
Norazlin Kamal Nor ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Central Nervous System ◽  
Nervous System ◽  
Signaling Pathway ◽  
Immune Dysregulation ◽  
Autism Spectrum ◽  
Mtor Signaling ◽  
Spectrum Disorder ◽  
Mtor Signaling Pathway ◽  
And Function

Autism spectrum disorder (ASD) is a heterogeneous, behaviorally defined, neurodevelopmental disorder that has been modeled as a brain-based disease. The behavioral and cognitive features of ASD are associated with pervasive atypicalities in the central nervous system (CNS). To date, the exact mechanisms underlying the pathophysiology of ASD still remain unknown and there is currently no cure or effective treatment for this disorder. Many publications implicated the association of ASD with inflammation, immune dysregulation, neurotransmission dysfunction, mitochondrial impairment and cell signaling dysregulation. This review attempts to highlight evidence of the major pathophysiology of ASD including abnormalities in the brain structure and function, neuroglial activation and neuroinflammation, glutamatergic neurotransmission, mitochondrial dysfunction and mechanistic target of rapamycin (mTOR) signaling pathway dysregulation. Molecular and cellular factors that contributed to the pathogenesis of ASD and how they may affect the development and function of CNS are compiled in this review. However, findings of published studies have been complicated by the fact that autism is a very heterogeneous disorder; hence, we addressed the limitations that led to discrepancies in the reported findings. This review emphasizes the need for future studies to control study variables such as sample size, gender, age range and intelligence quotient (IQ), all of which that could affect the study measurements. Neuroinflammation or immune dysregulation, microglial activation, genetically linked neurotransmission, mitochondrial dysfunctions and mTOR signaling pathway could be the primary targets for treating and preventing ASD. Further research is required to better understand the molecular causes and how they may contribute to the pathophysiology of ASD.

scholarly journals Forming learning skills of the child with autism spectrum disorder, organic damage of the central nervous system and intellectual deficits

2016 ◽  
Vol 14 (1) ◽  
pp. 49-56
Author(s):  
R.K. Ulianova ◽  
K.N. Ulianov
Keyword(s):  
Autism Spectrum Disorder ◽  
Central Nervous System ◽  
Nervous System ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Special Education Services ◽  
Educational Work ◽  
Learning Skills ◽  
The Central Nervous System ◽  
Intellectual Deficits

One of the most difficult stages of special education services for the child with autism spectrum disorder is establishing contact. When this problem is solved, a skilled educator would be able to reveal potential abilities and see a special interest (even maybe of a pathologic nature) even in a child with intellectual deficits. These interests and abilities are the basis of the further work on the child's development. This article describes the prolonged educational work during the 1970s on the preparation for school of a girl diagnosed with autism, organic damage of the central nervous system, diminished intellect, heightened aggression and impulsive be­havior. The article provides detailed description of the techniques used by the special educator for the problem solving, as well as general commentary for the concrete situations of the sessions with the child, the results of the work on developing learning skills and raising a child.

scholarly journals GCT-67. CENTRAL NERVOUS SYSTEM GERMINOMA IN TWO CAUCASIAN AMERICAN SIBLINGS WITH AUTISM SPECTRUM DISORDER

2020 ◽  
Vol 22 (Supplement_3) ◽  
pp. iii342-iii342
Author(s):  
Stephanie Toll ◽  
Hamza Gorsi
Keyword(s):  
Autism Spectrum Disorder ◽  
Central Nervous System ◽  
Nervous System ◽  
Klinefelter Syndrome ◽  
Germ Cell Tumors ◽  
Tumor Development ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Chromosomal Microarray ◽  
Caucasian American

Abstract BACKGROUND Central nervous system germ cell tumors (CNS-GCT) account for approximately 5% of all pediatric brain tumors. These tumors are pathologically heterogeneous, but have recurrent somatic mutations in KIT and rare germline variants in a Japanese cohort. Chromosomal abnormalities, specifically Klinefelter Syndrome, are associated with increased tumor development and familial cases have been reported, but no germline tumor syndromes are known. We describe a pair of siblings, both with autism spectrum disorder (ASD) that developed CNS-GCT, which previously has not been described outside of Japan. CASES: We report two siblings with ASD who developed CNS germinomas within two months of each other. The older brother, with basal ganglia and hypothalamic tumors, underwent surgical resection followed by treatment per ACNS0232 with chemotherapy and whole-ventricular irradiation (WVI). The younger sibling, with a midbrain tumor, also received ACNS0232, but due to poor response required additional chemotherapy and WVI. Both siblings are without evidence of disease 7 years after end of therapy. Genetic testing, including chromosomal microarray, karyotyping, and whole genome sequencing did not elucidate any variant identified as causative at that time. CONCLUSIONS CNS-GCT are rare tumors, diverse in both histopathologic diagnosis and clinical outcomes. Currently there are known somatic alterations and germline chromosomal disorders associated with increased tumor development, but no known inheritable causes. Despite this, familial CNS-GCT have been reported in patients of Japanese descent. The description of two Caucasian American siblings with ASD and CNS-GCT is novel, refuting that familial CNS-GCT are limited to the Japanese population.

scholarly journals Beta-adrenergic antagonism alters functional connectivity during associative processing in a preliminary study of individuals with and without autism

Autism ◽  
2019 ◽  
Vol 24 (3) ◽  
pp. 795-801
Author(s):  
John P Hegarty ◽  
Rachel M Zamzow ◽  
Bradley J Ferguson ◽  
Shawn E Christ ◽  
Eric C Porges ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Functional Connectivity ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Semantic Fluency ◽  
Beta Adrenergic ◽  
Associative Processing ◽  
The Brain

Beta-adrenergic antagonism (e.g. propranolol) has been associated with cognitive/behavioral benefits following stress-induced impairments and for some cognitive/behavioral domains in individuals with autism spectrum disorder. In this preliminary investigation, we examined whether the benefits of propranolol are associated with functional properties in the brain. Adolescents/adults (mean age = 22.54 years) with (n = 13) and without autism spectrum disorder (n = 13) attended three sessions in which propranolol, nadolol ( beta-adrenergic antagonist that does not cross the blood–brain barrier), or placebo was administered before a semantic fluency task during functional magnetic resonance imaging. Autonomic nervous system measures and functional connectivity between language/associative processing regions and within the fronto-parietal control, dorsal attention, and default mode networks were examined. Propranolol was associated with improved semantic fluency performance, which was correlated with the baseline resting heart rate. Propranolol also altered network efficiency of regions associated with semantic processing and in an exploratory analysis reduced functional differences in the fronto-parietal control network in individuals with autism spectrum disorder. Thus, the cognitive benefits from beta-adrenergic antagonism may be generally associated with improved information processing in the brain in domain-specific networks, but individuals with autism spectrum disorder may also benefit from additional improvements in domain-general networks. The benefits from propranolol may also be able to be predicted from baseline autonomic nervous system measures, which warrants further investigation.

Sign in / Sign up

Export Citation Format

Share Document