Ikran Mahad

From Genes to Behaviour: The Role of Neuroepigenetics in ADHD and dyslexia

Started May 17, 2024

Abstract or project description

Attention-deficit/hyperactivity disorder (ADHD) and dyslexia are two common neurodevelopmental disorders that significantly impact individuals' lives. ADHD is characterized by inattention, hyperactivity, and impulsivity, while dyslexia involves difficulties with language and reading abilities. Despite their distinct symptoms, both conditions are believed to be caused by a combination of genetic and environmental factors. Although typically identified in childhood, these conditions are thought to originate in utero. This projcet explores how genetic and environmental factors, along with trauma, interact at the molecular level to affect brain development and behaviour, with a focus on specific brain regions and the role of trauma in ADHD and dyslexia.

Moreover, acknowledging that genetic predispositions play a significant role in the development of ADHD and dyslexia. This project will highlight some studies. For instance, research has identified various genes associated with these conditions. For example, ADHD has been linked to genes involved in dopamine regulation which influence attention and behaviour. Similarly, dyslexia has been associated with genes which are involved in reading and language processing.

However, genetic factors alone do not account for the complexity of ADHD and dyslexia. Environmental factors also play a role. Prenatal exposure to toxins, maternal stress, and perinatal complications can all contribute to the risk of developing these disorders. Postnatal factors, including early childhood experiences, education, and family environment, further interact with genetic predispositions to shape the development of ADHD and dyslexia.

In addition to that trauma is a significant environmental factor that can worsen the symptoms of ADHD and dyslexia. Traumatic experiences, such as abuse, neglect, and stressors, can have effects on brain development and function. Trauma can disrupt the normal development of brain regions involved in emotion regulation and cognitive processing, which are often impaired in individuals with ADHD and dyslexia.

Research has shown that trauma can lead to changes in the structure and function of the prefrontal cortex, amygdala, and hippocampus—areas of the brain crucial for attention, memory, and emotional regulation. For example, children who have experienced trauma often show reduced prefrontal cortex volume and altered connectivity between the prefrontal cortex and other brain regions, contributing to difficulties with attention, impulse control, and emotional regulation, all hallmark features of ADHD.

In dyslexia, trauma can worsen difficulties with language and reading by impairing the brain's ability to process and integrate sensory information. Traumatic stress can lead to dysregulation of the visual processing pathways, making it harder for individuals with dyslexia to decode and comprehend written language. Moreover, the stress and anxiety resulting from trauma can further hinder academic performance and learning, creating a cycle of struggle and frustration.

It is also imperative to acknowledge the epigenetic mechanisms that provide a link between genetic predispositions, environmental influences, and the development of ADHD and dyslexia. Epigenetics involves changes in gene expression without altering the DNA sequence. These changes are often caused by environmental factors, including trauma, and can have lasting effects on brain development and behaviour.

One way trauma can impact gene expression is through DNA methylation, a process that adds methyl groups to DNA, typically silencing gene expression. This increased methylation can result in a stress response, making individuals more receptive to anxiety, depression, and difficulties with attention and executive function.

Another epigenetic mechanism influenced by trauma is histone modification. Histones are proteins around which DNA is wrapped, and their modification can either promote or repress gene expression. Trauma has been shown to alter histone acetylation and methylation patterns, affecting the expression of genes related to neural plasticity and cognitive function. These changes can impair the brain's ability to adapt and learn, contributing to the symptoms of ADHD and dyslexia.

Moreover, understanding the role of epigenetic modifications in these disorders opens up new ways for treatment. Epigenetic changes are reversible, and interventions that target these changes hold promise for reducing symptoms.

In conclusion, the complexity of ADHD and dyslexia involves a comprehensive understanding of the interplay between genetic predispositions, environmental influences, and trauma. By exploring how these factors interact at the molecular level, we can gain insights into the mechanisms driving these disorders and develop targeted interventions that address the unique challenges posed by each condition.