Dyslexia as an adaptation to cortico-limbic stress system reactivity

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 bra...

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Main Author: John R. Kershner
Format: Article
Language:English
Published: Elsevier 2020-05-01
Series:Neurobiology of Stress
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2352289520300138
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spelling doaj-79bbaa2713074b51a8785f2cf264a7312020-11-25T03:01:17ZengElsevierNeurobiology of Stress2352-28952020-05-0112Dyslexia as an adaptation to cortico-limbic stress system reactivityJohn R. Kershner0University of Toronto, Dept of Applied Psychology University of Toronto, Toronto, ON M5S 1A1, CanadaA 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.http://www.sciencedirect.com/science/article/pii/S2352289520300138DyslexiaStressEvolutionEpigeneticsNeuroplasticity
collection DOAJ
language English
format Article
sources DOAJ
author John R. Kershner
spellingShingle John R. Kershner
Dyslexia as an adaptation to cortico-limbic stress system reactivity
Neurobiology of Stress
Dyslexia
Stress
Evolution
Epigenetics
Neuroplasticity
author_facet John R. Kershner
author_sort John R. Kershner
title Dyslexia as an adaptation to cortico-limbic stress system reactivity
title_short Dyslexia as an adaptation to cortico-limbic stress system reactivity
title_full Dyslexia as an adaptation to cortico-limbic stress system reactivity
title_fullStr Dyslexia as an adaptation to cortico-limbic stress system reactivity
title_full_unstemmed Dyslexia as an adaptation to cortico-limbic stress system reactivity
title_sort dyslexia as an adaptation to cortico-limbic stress system reactivity
publisher Elsevier
series Neurobiology of Stress
issn 2352-2895
publishDate 2020-05-01
description 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.
topic Dyslexia
Stress
Evolution
Epigenetics
Neuroplasticity
url http://www.sciencedirect.com/science/article/pii/S2352289520300138
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