Abstract
Evolution fuels interindividual variability in neuroplasticity, reflected in brain anatomy and functional connectivity of the expanding neocortical regions subserving reading ability. Such variability is orchestrated by an evolutionarily conserved, competitive balance between epigenetic, stress-induced, and cognitive-growth gene expression programs. An evolutionary developmental model of dyslexia, suggests that prenatal and childhood subclinical stress becomes a risk factor for dyslexia when physiological adaptations to stress promoting adaptive fitness, may attenuate neuroplasticity in the brain regions recruited for reading. Stress has the potential to blunt the cognitive-growth functions of the predominantly right hemisphere Ventral and Dorsal attention networks, which are primed with high entropic levels of synaptic plasticity, and are critical for acquiring beginning reading skills. The attentional networks, in collaboration with the stress-responsive Default Mode network, modulate the entrainment and processing of the low frequency auditory oscillations (1–8 Hz) and visuospatial orienting linked etiologically to dyslexia. Thus, dyslexia may result from positive, but costly adaptations to stress system dysregulation: protective measures that reset the stress/growth balance of processing to favor the Default Mode network, compromising development of the attentional networks. Such a normal-variability conceptualization of dyslexia is at odds with the frequent assumption that dyslexia results from a neurological abnormality. To put the normal-variability model in the broader perspective of the state of the field, a traditional evolutionary account of dyslexia is presented to stimulate discussion of the scientific merits of the two approaches.
Highlights
An evolutionary developmental understanding of early childhood challenges the assumptions that reading disability and the effects of stress are both typically associated with neurological abnormalities
Dyslexia, and Stress during typical child development contradicts the view sometimes exhibited in research and clinical studies that individuals with dyslexia are suffering from a pathopsysiological condition
The results demonstrated that the frontoparietal network (FPN), ventral attention (VAN), and dorsal attention (DAN) combined to make up 56% of the brain’s reading network activations
Summary
An evolutionary developmental understanding of early childhood challenges the assumptions that reading disability and the effects of stress are both typically associated with neurological abnormalities. The dynamic tradeoff between these programs is managed by top–down activation of the hypothalamic-pituitary-adrenal (HPA) system (McGowen and Mathews, 2018; Raymond et al, 2018) and the Locus coeruleus-norepinephrine (LC/NE) system (Mather et al, 2016; Glennon et al, 2019) The significance of this to Evo-Devo and dyslexia is that the HPA and LC/NE systems are stress reactive and, within normal limits, produce considerable interindividual response variability (Krugers et al, 2017; Ellis and Del Giudice, 2019; Schultz et al, 2019). Dyslexia in the normalvariability model is a dimensional disability shaped by selection for neuroplasticity, as opposed to a categorical abnormality associated with selection for patterns of brain oscillations
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