The Autism studies/research thread

Post Reply New Topic

Background
Autism spectrum disorders (ASDs) are a collection of neurological, psychological, and developmental anomalies that manifest in early life, affecting individuals across all racial, cultural, and socioeconomic groups. Its prevalence has grown significantly over the past 20 years. Exposure to digital devices has increased alongside the rise in ASD prevalence. Research suggests that prolonged screen time can negatively impact a child's brain development, language, literacy, and cognitive function. The aim of this study was to investigate the correlation between screen time and the probability of developing autism spectrum disorder.

Methodology
This study employed a case-control design to examine 231 children in Zakho City diagnosed with an autism spectrum disorder. The study was conducted from October 1, 2023, to March 1, 2024. The participants included neurotypical individuals and individuals with autism. Data were gathered through standardized questionnaires and analyzed using IBM SPSS Statistics for Windows, Version 26 (Released 2019; IBM Corp., Armonk, New York). The study was approved by the College of Medicine/University of Zakho, Kurdistan Region, Iraq, and ethical permission was obtained.

Results
The study revealed a uniform age distribution between cases and controls, with a majority of male participants and a smaller percentage of female participants. ASD patients had a significantly longer duration of exposure to electronic devices compared to controls, with cases averaging 3.61 hours of screen time daily (t-test: t = 0.0001).

Conclusion
In summary, screens have a major impact on children's neurodevelopment and may increase their risk of developing ASD. However, no appreciable distinction was observed between children diagnosed with ASD and those without regarding early exposure to screens. Our findings can be used to create guidelines for children's media consumption and to raise awareness of this issue. Further research is needed to evaluate the association.

Summary: A new review highlights how air pollution, particularly fine particles and nitrogen oxides, can elevate autism risk by disrupting critical brain development processes. Key mechanisms, including nitrosative stress, neuroinflammation, and neurotransmitter disruptions, reveal how prenatal and early childhood exposure impact neurological health.

Small particles, such as PM2.5, can cross the placenta, potentially harming fetal brain development, especially for genetically predisposed individuals. The findings underscore an urgent need for protective measures for pregnant women in high-pollution areas. This research suggests cities may need to adapt urban planning to safeguard vulnerable populations.

Key Facts:
PM2.5 and NO products can cross the placenta, affecting fetal brain development.
Genetic predisposition to autism may increase vulnerability to air pollution.
Nitrosative stress, neuroinflammation, and endocrine disruption are key mechanisms.

The study reveals how common air pollutants, including fine particulate matter and nitrogen oxides, can trigger complex biological cascades affecting brain development.

“Different kinds of neurological disorders, including autism spectrum disorder, can be associated with this environmental factor,” explains Professor Haitham Amal from the Hebrew University of Jerusalem, the study’s senior author.

“The timing of exposure appears crucial, with heightened vulnerability during prenatal development and early childhood when critical neurodevelopmental processes occur.”

The review identifies several key pathways through which air pollutants may influence ASD development:

Nitrosative stress orchestrated by nitric oxide (NO)

• Neuroinflammation and oxidative stress

• Disruption of neurotransmitter systems

• Epigenetic modifications

• Endocrine system interference

• Metabolic pathway dysregulation

Of particular concern is the finding that smaller particles, especially PM2.5 as well as NO products, can cross the placenta and affect fetal brain development. This revelation raises important questions about protective measures for pregnant women in highly polluted areas.

“The research suggests that individuals with genetic predisposition to ASD may be more vulnerable to the harmful effects of air pollution exposure,” Professor Amal notes. “This interaction between genetic and environmental factors opens new avenues for understanding ASD’s complex etiology.”

My lab has shown that NO plays a major role in ASD. However, this study emphasizes the critical role of this molecule and its derivatives on the brain” Prof. Amal comments.

The review, first authored by PhD student Shashank Ojha, also highlights promising directions for biomarker development, potentially enabling early identification of at-risk individuals. These findings arrive at a crucial time, as global ASD prevalence reaches 1-1.5% of the population.

The implications extend beyond individual health to public policy. How might cities need to adapt their urban planning to protect vulnerable populations? What role could air quality monitoring play in prenatal care? These questions become increasingly urgent as urbanization continues worldwide.

The research team emphasizes the need for comprehensive studies examining the combined effects of multiple pollutants, particularly during specific developmental windows. Understanding these interactions could prove crucial for developing effective preventive strategies.

Background
Based on the Interaction of Person-Affect-Cognition-Execution (I-PACE) model, this study aimed to explore the relationship between autistic traits and problematic smartphone use (PSU) among Chinese adolescents and to examine the serial mediation effect of anxiety and executive dysfunction in the association between autistic traits and PSU.

Methods
The Autism-Spectrum Quotient, Smartphone Addiction Scale, the trait version of the State–Trait Anxiety Inventory, and Dysexecutive Questionnaire were administered to a sample comprising 412 senior high school students (average age = 17.05 years, SD = 0.65). Structural equation models were utilized to explore the simple and serial mediating role of anxiety and executive dysfunction played in the association between autistic traits and PSU.

Results
This study found that social rather than non-social autistic traits were positively associated with anxiety, executive dysfunction, and PSU. Furthermore, after controlling for gender, anxiety and executive dysfunction acted as sequential mediators in the connection between social autistic trait and PSU. However, non-social autistic trait did not predict anxiety, executive dysfunction, or PSU.

Conclusion
This study supports the I-PACE model and deepens understanding of PSU formation. Furthermore, the findings underscore the importance of addressing social challenges faced by adolescents with high autistic traits, providing a viable potential intervention pathway to promote healthy smartphone use in this population.

A study from Tel Aviv University expands the understanding of the biological mechanism underlying genetically-based autism, specifically mutations in the SHANK3 gene, responsible for nearly one million cases of autism worldwide. Based on these discoveries, the research team applied a genetic treatment that improved the function of cells affected by the mutation, laying a foundation for future treatments for SHANK3-related autism.

The study was led by the lab of Prof. Boaz Barak and Ph.D. student Inbar Fischer from the Sagol School of Neuroscience and the School of Psychological Sciences at Tel Aviv University, in collaboration with the labs of Prof. Ben Maoz from the Department of Biomedical Engineering at Fleischman Faculty of Engineering at Tel Aviv University and Prof. Shani Stern from the Department of Neurobiology at the University of Haifa. The article was published in the journal Science Advances.

Prof. Barak says, "Autism is a relatively common neurodevelopmental disorder. According to current data, 1–2% of the global population and one in every 36 boys in the U.S. are diagnosed with autism spectrum disorder (ASD), with numbers rising over time. Autism is caused by a wide range of factors—environmental, genetic, and even social and cultural (such as the rise in parental age at conception). In my lab, we study genetic causes of autism.

"Among these, mutations in a gene called SHANK3. The impact of these mutations on the function of brain neurons has been extensively studied, and we know that the protein encoded by SHANK3 plays a central role in binding receptors in the neuron, essential for receiving chemical signals (neurotransmitters and others) by which neurons communicate

Thus, damage to this gene can disrupt message transmission between neurons, impairing the brain's development and function. In this study we sought to shed light on other, previously unknown mechanisms, through which mutations in the SHANK3 gene disrupt brain development, leading to disorders manifested as autism."

Specifically, the research team focused on two components in the brain not yet studied extensively in this context: non-neuronal brain cells (glia) called oligodendrocytes and the myelin they produce. Myelin tissue is a fatty layer that insulates nerve fibers (axons), similar to the insulating layer that coats electrical cables. When the myelin is faulty, the electrical signals transmitted through the axons may leak, disrupting the message transmission between brain regions and impairing brain function.

The team employed a genetically engineered mouse model for autism, introducing a mutation in the Shank3 gene that mirrors the mutation found in humans with this form of autism.

Fischer said, "Through this model, we found that the mutation causes a dual impairment in the brain's development and proper function: first, in oligodendrocytes, as in neurons, the SHANK3 protein is essential for the binding and functioning of receptors that receive chemical signals (neurotransmitters and others) from neighboring cells. This means that the defective protein associated with autism disrupts message transmission to these vital support cells.

"Secondly, when the function and development of oligodendrocytes is impaired, their myelin production is also disrupted. The faulty myelin does not properly insulate the neuron's axons, thereby reducing the efficiency of electrical signal transmission between brain cells, as well as the synchronization of electrical activity between different parts of the brain. In our model, we found myelin impairment in multiple brain areas and observed that the animals' behavior was adversely affected as a result."

The researchers then sought a method for fixing the damage caused by the mutation, with the hope of ultimately developing a treatment for humans.

Fischer explained, "We obtained oligodendrocytes from the brain of a mouse with a Shank3 mutation, and inserted DNA segments containing the normal human SHANK3 sequence. Our goal was to allow the normal gene to encode a functional and normal protein, which, replacing the defective protein, would perform its essential role in the cell.

"To our delight, following treatment, the cells expressed the normal SHANK3 protein, enabling the construction of a functional protein substrate to bind the receptors that receive electrical signals. In other words, the genetic treatment we had developed repaired the oligodendrocytes' communication sites, essential for the cells' proper development and function as myelin producers."

To validate findings from the mouse model, the research team generated induced pluripotent stem cells from skin cells of a girl with autism caused by a SHANK3 gene mutation identical to that in the mice. From these stem cells, they derived human oligodendrocytes with the same genetic profile. These oligodendrocytes displayed impairments similar to those observed in their mouse counterparts.

Abstract
Individuals diagnosed with autism spectrum disorder (ASD) show neural and behavioral characteristics differing from the neurotypical population. This may stem from a computational principle that relates inference and computational dynamics to the dynamic range of neuronal population responses, reflecting the signal levels for which the system is responsive. In the present study, we showed that an increased dynamic range (IDR), indicating a gradual response of a neuronal population to changes in input, accounts for neural and behavioral variations in individuals diagnosed with ASD across diverse tasks. We validated the model with data from finger-tapping synchronization, orientation reproduction and global motion coherence tasks. We suggested that increased heterogeneity in the half-activation point of individual neurons may be the biological mechanism underlying the IDR in ASD. Taken together, this model provides a proof of concept for a new computational principle that may account for ASD and generates new testable and distinct predictions regarding its behavioral, neural and biological foundations.

Can anyone translate that to simpler English?

Can anyone translate that to simpler English?

Abstract
Alterations and maladaptation of the immune system remain some of the most controversial concepts in autism spectrum disorder (ASD). Nonetheless, intensifying evidence confirms that much of what ASD involves is related not to fixed “autistic states of being” but rather to the consequences of environmental insult and complex psychological and physiological processes along a neuro-immune-microbiota-axis. Beginning with an epidemiological and etiological underpinning, followed by biochemical and psychiatric standpoints, we elaborate on the current role of the immune system in the pathophysiology of ASD. Finally, taking a neuroimmunological perspective, we highlight the need for a multi-scale, holistic, and “middle-out” approach to understanding and developing future therapeutic modalities to address the core symptoms of ASD that go beyond the current reductionist and “magic-bullet” medical paradigm.