Kershner-2020

A new school of thought in evolutionary developmental biology, combined with research in the neurobiology of stress, suggest that early exposure to stressful circumstances may be a cause of dyslexia. A balance between epigenetic, stress-induced and cognitive-growth genetic programs modulates the brain’s cellular, regional, and network homeostasis. This balance is essential for adaptability to the normative range of everyday stress. However, even mild chronic stress exposition may overactivate the hypothalmic-pituitary-adrenal stress axis, upsetting the homeostatic balance between these programs, and exposing the brain to harmful levels of stress hormones. A protective strategy to sustained disequilibrium precociously advances maturation at the cost of neuroplasticity, which blunts stress axis reactivity but also compromises learning potential in the prefrontal cortex and networks associated with dyslexia. Stress exceeding an individual’s range of resilience: (1) reduces levels of TFEB and BDNF, gene regulatory factors prolonging maturation and neuroplasticity; (2) interferes with the insular cortex, amygdala and hippocampus in coordinating afferent visceral signals with cognitive performance; (3) over-recruits the brain’s Default Mode network; and (4) amplifies release from the Locus coeruleus/norepinephrine system which impairs the entrainment of oscillations in the lower phonological frequencies of speech. Evidence supporting a stress-growth imbalance is preliminary, but holds promise for reconceptualizing the neurobiology of dyslexia and reducing its prevalence.