scholarly journals Valproic Acid in Autism Spectrum Disorder: From an Environmental Risk Factor to a Reliable Animal Model

10.5772/54824 ◽  
2013 ◽  
Author(s):  
Carmem Gottfried ◽  
Victorio Bambini-Junior ◽  
Diego Baronio ◽  
Geancarlo Zanatta ◽  
Roberta Bristot ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Valproic Acid ◽  
Animal Model ◽  
Risk Factor ◽  
Environmental Risk ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Environmental Risk Factor

scholarly journals What We Have Learned about Autism Spectrum Disorder from Valproic Acid

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Taylor Chomiak ◽  
Nathanael Turner ◽  
Bin Hu
Keyword(s):  
Autism Spectrum Disorder ◽  
Valproic Acid ◽  
Animal Model ◽  
Neurodevelopmental Disorders ◽  
Significant Risk ◽  
Autism Spectrum ◽  
Research Literature ◽  
Spectrum Disorder ◽  
Epidemiological Evidence ◽  
Growing Body

Two recent epidemiological investigations in children exposed to valproic acid (VPA) treatment in utero have reported a significant risk associated with neurodevelopmental disorders and autism spectrum disorder (ASD) in particular. Parallel to this work, there is a growing body of animal research literature using VPA as an animal model of ASD. In this focused review we first summarize the epidemiological evidence linking VPA to ASD and then comment on two important neurobiological findings linking VPA to ASD clinicopathology, namely, accelerated or early brain overgrowth and hyperexcitable networks. Improving our understanding of how the drug VPA can alter early development of neurological systems will ultimately improve our understanding of ASD.

scholarly journals Preliminary Results Regarding Sleep in a Zebrafish Model of Autism Spectrum Disorder

2021 ◽  
Vol 11 (5) ◽  
pp. 556
Author(s):  
Madalina Andreea Robea ◽  
Alin Ciobica ◽  
Alexandrina-Stefania Curpan ◽  
Gabriel Plavan ◽  
Stefan Strungaru ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Valproic Acid ◽  
Social Behavior ◽  
Antiepileptic Drug ◽  
Alternative Model ◽  
Neurological Diseases ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Zebrafish Model ◽  
Developmental Defects

Autism spectrum disorder (ASD) is one of the most salient developmental neurological diseases and remarkable similarities have been found between humans and model animals of ASD. A common method of inducing ASD in zebrafish is by administrating valproic acid (VPA), which is an antiepileptic drug that is strongly linked with developmental defects in children. In the present study we replicated and extended the findings of VPA on social behavior in zebrafish by adding several sleep observations. Juvenile zebrafish manifested hyperactivity and an increase in ASD-like social behaviors but, interestingly, only exhibited minimal alterations in sleep. Our study confirmed that VPA can generate specific ASD symptoms, indicating that the zebrafish is an alternative model in this field of research.

scholarly journals Alterations of the endocannabinoid system and its therapeutic potential in autism spectrum disorder

Open Biology ◽  
2021 ◽  
Vol 11 (2) ◽  
Author(s):  
Mingyang Zou ◽  
Yu Liu ◽  
Shu Xie ◽  
Luxi Wang ◽  
Dexin Li ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Animal Model ◽  
Social Preference ◽  
Therapeutic Potential ◽  
Hydrolytic Enzyme ◽  
Endocannabinoid System ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Autistic Children ◽  
Novel Approach

Autism spectrum disorder (ASD) is a group of developmental disabilities, the aetiology of which remains elusive. The endocannabinoid (eCB) system modulates neurotransmission and neuronal plasticity. Evidence points to the involvement of this neuromodulatory system in the pathophysiology of ASD. We investigated whether there is a disruption to the eCB system in ASD and whether pharmacological modulation of the eCB system might offer therapeutic potential. We examined three major components of the eCB system—endogenous cannabinoids, their receptors and associated enzymes—in ASD children as well as in the valproic acid (VPA) induced animal model in autism. Furthermore, we specifically increased 2-arachidonoylglycerol (2-AG) levels by administering JZL184, a selective inhibitor of monoacylglycerol lipase which is the hydrolytic enzyme for 2-AG, to examine ASD-like behaviours in VPA-induced rats. Results showed that autistic children and VPA-induced rats exhibited reduced eCB content, increased degradation of enzymes and upregulation of CBRs. We found that repetitive and stereotypical behaviours, hyperactivity, sociability, social preference and cognitive functioning improved after acute and chronic JZL184 treatment. The major efficacy of JZL184 was observed after administration of a dosage regimen of 3 mg kg −1 , which affected both the eCB system and ASD-like behaviours. In conclusion, a reduced eCB signalling was observed in autistic children and in the ASD animal model, and boosting 2-AG could ameliorate ASD-like phenotypes in animals. Collectively, the results suggested a novel approach to ASD treatment.

scholarly journals The Untouchable Ventral Nucleus of the Trapezoid Body: Preservation of a Nucleus in an Animal Model of Autism Spectrum Disorder

2021 ◽  
Vol 15 ◽  
Author(s):  
Yusra Mansour ◽  
Randy J. Kulesza
Keyword(s):  
Autism Spectrum Disorder ◽  
Animal Model ◽  
Autism Spectrum ◽  
Repetitive Behaviors ◽  
Spectrum Disorder ◽  
Superior Olivary Complex ◽  
Medial Geniculate ◽  
Ventral Nucleus ◽  
Descending Projections ◽  
Trapezoid Body

Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by repetitive behaviors, poor social skills, and difficulties with communication and hearing. The hearing deficits in ASD range from deafness to extreme sensitivity to routine environmental sounds. Previous research from our lab has shown drastic hypoplasia in the superior olivary complex (SOC) in both human cases of ASD and in an animal model of autism. However, in our study of the human SOC, we failed to find any changes in the total number of neurons in the ventral nucleus of the trapezoid body (VNTB) or any changes in cell body size or shape. Similarly, in animals prenatally exposed to the antiepileptic valproic acid (VPA), we failed to find any changes in the total number, size or shape of VNTB neurons. Based on these findings, we hypothesized that the neurotransmitter profiles, ascending and descending axonal projections of the VNTB are also preserved in these neurodevelopmental conditions. We investigated this hypothesis using a combination of immunohistochemistry and retrograde tract tracing. We found no difference between control and VPA-exposed animals in the number of VNTB neurons immunoreactive for choline acetyltransferase (ChAT). Additionally, we investigated the ascending projections from the VNTB to both the central nucleus of the inferior colliculus (CNIC) and medial geniculate (MG) and descending projections to the cochlea. Our results indicate no significant differences in the ascending and descending projections from the VNTB between control and VPA-exposed animals despite drastic changes in these projections from surrounding nuclei. These findings provide evidence that certain neuronal populations and circuits may be protected against the effects of neurodevelopmental disorders.

scholarly journals Hypovitaminosis D as a risk factor for severe autism spectrum disorder

2021 ◽  
Vol 61 (2) ◽  
pp. 82-8
Author(s):  
Diyah Rakanita Undang ◽  
Mei Neni Sitaresmi ◽  
Roni Naning
Keyword(s):  
Autism Spectrum Disorder ◽  
Vitamin D ◽  
Risk Factor ◽  
General Hospital ◽  
Parental Education ◽  
Hypovitaminosis D ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Children With Asd ◽  
Vitamin D Levels

Background Vitamin D is an important risk factor for autism spectrum disorder (ASD). However, research on hypovitaminosis D as a risk factor for severe ASD  has been limited. To our knowledge, no such studies have been done in Indonesia. Objective To evaluate hypovitaminosis D as a risk factor for severe ASD. Methods This cross-sectional study included children aged 2-18 years who fulfilled the ASD DSM-5 diagnostic criteria. Subjects were consecutively sampled from April - June 2019 at the Child Growth and Polyclinic, Dr. Sardjito General Hospital, Yogyakarta. Assessment of ASD severity was carried out using the Childhood Autism Rating Scale Second Edition (CARS-2) questionnaire. Serum 25(OH)D examination was done in the Clinical Laboratory, Dr. Sardjito General Hospital.  Results Of 36 children with ASD, 36.1% had hypovitaminosis D (<30 ng/mL) and 69.4% had severe ASD, based on the CARS-2 questionnaire (≥37-60). Bivariate analysis revealed that children with hypovitaminosis D had more severe CARS-2 values ​​(92.3%) compared to those with normal vitamin D levels (56.5%) (PR 1.633; 95%CI 1.10 to 2.42; P=0.031). Multivariate analysis with logistic regression revealed that hypovitaminosis D increased the risk of severe ASD (PR 1.65; 95%CI 1.06 to 2.56; P=0.037). However, other variables such as gender, parental education, attention deficit and hyperactivity disorder (ADHD), epilepsy, sleep disorders, pharmacotherapy and non-pharmacotherapy had no significant relationships with severe ASD. Conclusion Children with ASD and hypovitaminosis D have a 1.65 times higher risk of severe ASD compared to children with ASD and sufficient vitamin D levels. We recommend that children with ASD undergo serum 25(OH)D monitoring.

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