A study found significant overlaps between various environmental pollutants and dyslexia susceptibility genes, identifying associations with 35 out of 95 chemicals.
This suggests that these chemicals may contribute to the development of dyslexia through interactions with specific genes.
Highlights:
- Dyslexia Risk Genes & Chemicals: The study identified 131 dyslexia susceptibility genes and examined their interactions with 95 environmental chemicals, finding significant overlap with 35 of these chemicals.
- Chemical Enrichment: Significant enrichment values for dyslexia risk genes were found with chemicals such as atrazine and dibenzo(a, h)pyrene, indicating a strong chemical bias towards these genes.
- Metal Involvement: Metals like chromium, manganese, cobalt, copper, zinc, arsenic, selenium, and mercury showed significant enrichment values in relation to dyslexia risk genes, suggesting a potential role in dyslexia development.
- Persistent Organic Pollutants (POPs): Five POPs, including chlordane, dichlorodiphenyl trichloroethane, and dieldrin, displayed significant biases towards dyslexia-associated genes.
- Pesticides & Dyslexia: Various pesticides, including glyphosate, lambda-cyhalothrin, permethrin, and chlorpyrifos, were more likely to act on dyslexia risk genes, indicating their potential involvement in the disorder’s pathogenesis.
Source: BMC Psychiatry (2024)
Major Findings: Dyslexia Genes vs. Environmental Pollutants (2024 Analysis)
Yang et al. evaluated the interaction between dyslexia risk genes and environmental chemicals and pollutants to determine whether environment may modify these genes and dyslexia risk – below are the main findings.
1. Chemical Enrichment & Dyslexia Risk Genes
The study identified significant overlaps between environmental chemicals and dyslexia susceptibility genes.
Out of 95 chemicals analyzed, 35 showed a noteworthy association with genes linked to dyslexia.
Key Chemicals: Atrazine and dibenzo(a, h)pyrene were among the chemicals with the highest enrichment values, indicating a strong likelihood of interaction with dyslexia-related genes.
Implications: These findings suggest that certain chemicals might influence the development of dyslexia by interacting with specific genetic markers.
2. Metals & Their Impact
The study highlighted several metals that showed significant enrichment values in relation to dyslexia risk genes.
Key Metals: Chromium, manganese, cobalt, copper, zinc, arsenic, selenium, and mercury were all found to have a strong association with dyslexia genes.
Details: For example, manganese, which had a significant enrichment value, is known for its neurotoxic effects. High levels of exposure can lead to cognitive impairments and developmental issues. Similarly, lead exposure has been linked to reduced cognitive function and behavioral problems in children.
Implications: These metals could affect brain development by altering gene expression, damaging neurons, and disrupting synaptic connections.
3. Persistent Organic Pollutants (POPs) & Dyslexia
The study found significant biases towards dyslexia risk genes in relation to several POPs.
Key POPs: Chemicals like chlordane, dichlorodiphenyl trichloroethane (DDT), dieldrin, heptachlor, and toxaphene showed notable enrichment values.
Details: For instance, DDT has been linked to poorer cognitive function and developmental delays in children. These chemicals can affect the nervous system by disrupting hormonal functions and causing oxidative stress, which can lead to neurodevelopmental disorders.
Implications: The association between POPs and dyslexia suggests that exposure to these chemicals during critical developmental periods could increase the risk of developing the disorder. This highlights the need for stricter regulations and monitoring of POPs in the environment.
4. Polycyclic Aromatic Hydrocarbons (PAHs) & Cognitive Function
Several PAHs were found to have significant biases towards dyslexia risk genes.
Key PAHs: Anthracene and phenanthrene were among the PAHs with strong associations.
Details: PAHs are by-products of burning fossil fuels and can affect brain development by reducing levels of brain-derived neurotrophic factor (BDNF), which is crucial for neuronal growth and cognitive function. Reduced BDNF levels can lead to impaired learning and memory.
Implications: Exposure to PAHs might disrupt normal brain development and contribute to cognitive deficits seen in dyslexia. This underscores the importance of minimizing exposure to these pollutants, especially in children.
5. Pesticides & Their Role in Dyslexia
The analysis revealed significant biases towards dyslexia-related genes in several pesticides.
Key Pesticides: Glyphosate, lambda-cyhalothrin, permethrin, and chlorpyrifos were among the pesticides showing notable enrichment values.
Details: Glyphosate, for example, can affect synaptic transmission and induce biochemical changes that impair cognitive functions. Other pesticides, like chlorpyrifos, can inhibit cholinesterase activity, disrupting nerve signal transmission and causing developmental issues.
Implications: The findings suggest that pesticide exposure could be a risk factor for dyslexia by altering gene expression and damaging the nervous system. This calls for more stringent regulations on pesticide use and further research into safer alternatives.
Study Details: Overlap Between Dyslexia Genes & Environmental Pollutants (2024)
The study aimed to systematically explore the overlap between exposure to environmental compounds and susceptibility genes in the development of developmental dyslexia, to identify potential chemical contributors to the disorder.
Sample
The analysis included 131 publicly reported dyslexia susceptibility genes sourced from DisGeNET, OMIM, and GeneCards databases.
It also involved examining the overlap with 95 environmental compounds from the Comparative Toxicogenomics Database (CTD), including metals, persistent organic pollutants (POPs), polycyclic aromatic hydrocarbons (PAHs), and pesticides.
Methods
- Data Compilation: Susceptibility genes for dyslexia were collected from DisGeNET, OMIM, and GeneCards databases.
- Chemical-Gene Overlap Analysis: The CTD database was used to explore the overlap between susceptibility genes and environmental compounds.
- Statistical Analysis: The observation/expectation ratios and hypergeometric probability test were used to identify significant chemical biases towards dyslexia risk genes.
- Sensitivity Analysis: Restricted analysis to genes expressed in the brain, excluding non-relevant genes like STATH.
Limitations
- Scope of Chemicals: Only 95 environmental compounds were analyzed, potentially missing other relevant chemicals.
- Theoretical Analysis: The study was based on theoretical data and did not involve actual clinical research, limiting the clinical significance of the findings.
- Exploratory Nature: The findings are preliminary and require further validation through animal or cellular experiments to establish causal relationships.
- Gene Expression Data: The study focused on gene expression data, which may not fully capture the complex interactions and effects of environmental compounds on gene function.
How Environmental Chemicals & Pollutants May Cause Dyslexia (Mechanisms)
Neurotoxicity
Heavy Metals: Metals like lead, mercury, and arsenic are known neurotoxins. They can disrupt normal brain development by damaging neurons and interfering with synaptic function. For example, lead exposure has been linked to neurobehavioral deficits, such as reduced intelligence and attention, which are critical for reading and language skills.
Mechanism: These metals can induce oxidative stress, disrupt neurotransmitter functions, and interfere with the formation and maintenance of synaptic connections, all of which are essential for cognitive functions involved in reading and writing.
Endocrine Disruption
Persistent Organic Pollutants (POPs): Chemicals such as DDT, dieldrin, and heptachlor can interfere with hormone systems. Hormones like thyroid hormones are crucial for brain development and function.
Mechanism: These chemicals can disrupt thyroid function, leading to altered levels of thyroid hormones that are essential for brain development. This disruption can result in abnormal brain development, affecting cognitive functions related to dyslexia.
Oxidative Stress
Polycyclic Aromatic Hydrocarbons (PAHs): Compounds like benzo(a)pyrene and anthracene can induce oxidative stress in the brain. Oxidative stress damages cellular components, including DNA, proteins, and lipids.
Mechanism: The oxidative stress caused by PAHs can lead to neuronal damage and impairments in synaptic plasticity, which is vital for learning and memory. Reduced levels of brain-derived neurotrophic factor (BDNF), crucial for cognitive functions, have been associated with PAH exposure.
Inflammation & Immune Response
Pesticides: Chemicals such as glyphosate and chlorpyrifos can trigger inflammatory responses in the brain. Inflammation can disrupt normal brain development and function.
Mechanism: These pesticides can activate microglia and astrocytes, the brain’s immune cells, leading to the release of pro-inflammatory cytokines. Chronic inflammation can result in neuronal damage and disruptions in neural connectivity, which are critical for language processing and reading skills.
Genetic & Epigenetic Modifications
Chemical-Gene Interactions: Environmental chemicals can interact with dyslexia susceptibility genes, leading to changes in gene expression and function. For instance, zinc interacts with the GRIN2B gene, affecting learning and memory pathways.
Mechanism: Chemicals can cause mutations or epigenetic changes, such as DNA methylation and histone modification, which alter the expression of genes involved in brain development. These changes can impair neural circuits related to reading and language processing.
Disruption of Synaptic Plasticity
Neurotoxic Chemicals: Exposure to neurotoxic chemicals like copper and manganese can disrupt synaptic plasticity, the brain’s ability to strengthen or weaken synapses in response to activity.
Mechanism: These chemicals can interfere with signaling pathways, such as the Ras-MAPK/ERK pathway, crucial for synaptic plasticity. Disrupted synaptic plasticity can impair learning and memory, essential for reading skills.
Conclusion: Environmental Chemicals vs. Dyslexia Genes
This study systematically explored the potential links between environmental chemicals and dyslexia susceptibility genes, identifying significant overlaps that suggest these chemicals may contribute to the disorder’s development.
Key findings include the significant enrichment of dyslexia risk genes with chemicals such as metals, POPs, PAHs, and pesticides.
These chemicals can disrupt normal brain development through mechanisms like neurotoxicity, endocrine disruption, oxidative stress, inflammation, and genetic modifications.
While the findings provide valuable insights into the environmental factors contributing to dyslexia, they are exploratory and require further validation through animal and cellular experiments.
Understanding these mechanisms is crucial for developing effective prevention and intervention strategies to mitigate the impact of these chemicals on neurodevelopmental disorders like dyslexia.
References
- Study: Developmental dyslexia genes are selectively targeted by diverse environmental pollutants (2024)
- Authors: Yangyang Yang et al.
