Central Causation of Autism/ASDs via Excessive [Ca2+]i Impacting Six Mechanisms Controlling Synaptogenesis during the Perinatal Period: The Role of Electromagnetic Fields and Chemicals and the NO/ONOO(-) Cycle, as Well as Specific Mutations
Abstract
Overview
The study examines the interplay between perinatal development, intracellular calcium ([Ca2+]i), synaptogenesis, and the subsequent development of autism spectrum disorders (ASDs). Central to the hypothesis presented are six mechanisms regulated by [Ca2+]i, each aberrant in ASDs.
Findings
- Multiple Factors: Both electromagnetic fields (EMFs) and various chemicals play a role via voltage-gated calcium channel activation, leading to elevated [Ca2+]i. This is linked to autism by affecting key developmental processes such as neuronal migration, dendritic outgrowth, and synapse formation.
- Epigenetic & Genetic Elements: Chronic ASD conditions are explained by NO/ONOO(-) cycle elevation and MeCP2 epigenetic dysfunction, with genetic factors often involving similar pathways.
- Systematic Examination: Thorough review of literature confirms the model's consistency with existing predictions.
Conclusion
The paper proposes preventive and treatment approaches that include avoiding EMFs and harmful chemicals, utilizing nutrients to enhance Nrf2 levels, and maintaining an enriched environment with substances like vitamin D and omega-3 fatty acids.