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.

中文翻译：

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阅读障碍、压力和大脑网络稳态的进化视角

进化加剧了神经可塑性的个体差异，这反映在大脑解剖结构和不断扩大的新皮质区域的功能连接上，从而促进了阅读能力。这种变异性是由表观遗传、应激诱导和认知增长基因表达程序之间进化上保守的竞争性平衡精心策划的。阅读障碍的进化发展模型表明，当对压力的生理适应促进适应性适应性时，产前和儿童亚临床压力成为阅读障碍的危险因素，可能会削弱为阅读而招募的大脑区域的神经可塑性。压力有可能削弱主要是右半球腹侧和背侧注意力网络的认知生长功能，这些网络以高熵水平的突触可塑性为基础，对于获得开始阅读技能至关重要。注意力网络与压力响应默认模式网络合作，调节低频听觉振荡（1-8 Hz）的夹带和处理以及与阅读障碍病因相关的视觉空间定向。因此，阅读障碍可能是由于对压力系统失调进行积极但代价高昂的适应而导致的：重置处理的压力/生长平衡以有利于默认模式网络的保护措施，从而损害注意力网络的发展。这种对阅读障碍的正常变异性概念与阅读障碍是由神经异常引起的常见假设不一致。为了将正常变异模型置于该领域的更广阔的视野中，提出了阅读障碍的传统进化解释，以激发对这两种方法的科学优点的讨论。