Suggestion of a dynamic model of the development of neurodevelopmental disorders and the phenomenon of autism

Bodil Aggernæs ^{1,2
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1.
Department of Child and Adolescent Psychiatry, Psychiatry Region Zealand, 4000 Roskilde, Denmark; Department of Clinical Medicine, Faculty of Medical and Health Sciences, University of Copenhagen, 2200 Copenhagen N, Denmark
2.
Department of Adult Psychiatry, Mental Health Centre Northern Zealand, Mental Health Services of the Capital Region, 3400 Hillerød, Denmark

Received: 14 January 2020 Accepted: 27 May 2020 Published: 29 May 2020

Abstract
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The present article is a theoretical contribution suggesting a simple model of the dynamics involved in the development of neurodevelopmental disorders and the phenomenon of autism offering an explanation of why different individuals have different onset of manifest disease. The model relates to present genetic and epigenetic evidence and previous theoretical models. The dynamic model applies an individualized transdiagnostic and dimensional approach integrating several levels of influence involved in the dynamic interaction between an individual and their environment across time. The dynamic model illustrates the interaction between a basic neurobiological susceptibility, compensating mechanisms, and stress-related releasing mechanisms involved in the development of manifest clinical illness. The model has a particular focus on the dynamics of neurocognitive processes and their relationship to more basic information, psychological and social processes. A basic assumption guiding the model is that even quite normal events related to typical development may increase the risk of enduring stress in cognitively vulnerable individuals, further increasing their risk of developing manifest clinical illness. The model suggests that genetic variation, endogenous epigenetic processes of development, and epigenetic changes influenced by physical/chemical and social environmental risk and resilience factors all may contribute to phenotypical expression. A genetic susceptibility may translate into a biological susceptibility reflected in cognitive impairments. A cognitively vulnerable individual may be at increased risk of misinterpreting sensory inputs, potentially resulting in psychopathological expressions, e.g., autistic symptoms, observed across several neurodevelopmental disorders. The genetically influenced experience of an individual relates to cognitive phenomena occurring at the interfaces between the brain, mind, and society. The severity of clinical illness may differ from the severity of a disorder of reasoning. The dynamic model may help guide future development of personalized medicine in psychiatry and identify relevant points of intervention. A discussion of the implications of the model relating to epigenetic evidence and to previous theoretical models is included at the end of the paper.
- molecular mechanisms,
- gene-environment,
- epigenetics,
- stress,
- vulnerability,
- neurocognitive impairments,
- experience,
- psychodynamics,
- social interaction,
- compensation
Citation: Bodil Aggernæs. Suggestion of a dynamic model of the development of neurodevelopmental disorders and the phenomenon of autism[J]. AIMS Molecular Science, 2020, 7(2): 122-182. doi: 10.3934/molsci.2020008

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Abstract

The present article is a theoretical contribution suggesting a simple model of the dynamics involved in the development of neurodevelopmental disorders and the phenomenon of autism offering an explanation of why different individuals have different onset of manifest disease. The model relates to present genetic and epigenetic evidence and previous theoretical models. The dynamic model applies an individualized transdiagnostic and dimensional approach integrating several levels of influence involved in the dynamic interaction between an individual and their environment across time. The dynamic model illustrates the interaction between a basic neurobiological susceptibility, compensating mechanisms, and stress-related releasing mechanisms involved in the development of manifest clinical illness. The model has a particular focus on the dynamics of neurocognitive processes and their relationship to more basic information, psychological and social processes. A basic assumption guiding the model is that even quite normal events related to typical development may increase the risk of enduring stress in cognitively vulnerable individuals, further increasing their risk of developing manifest clinical illness. The model suggests that genetic variation, endogenous epigenetic processes of development, and epigenetic changes influenced by physical/chemical and social environmental risk and resilience factors all may contribute to phenotypical expression. A genetic susceptibility may translate into a biological susceptibility reflected in cognitive impairments. A cognitively vulnerable individual may be at increased risk of misinterpreting sensory inputs, potentially resulting in psychopathological expressions, e.g., autistic symptoms, observed across several neurodevelopmental disorders. The genetically influenced experience of an individual relates to cognitive phenomena occurring at the interfaces between the brain, mind, and society. The severity of clinical illness may differ from the severity of a disorder of reasoning. The dynamic model may help guide future development of personalized medicine in psychiatry and identify relevant points of intervention. A discussion of the implications of the model relating to epigenetic evidence and to previous theoretical models is included at the end of the paper.

Abbreviation ASD: Autism Spectrum Disorders; CNV: Copy Number Variants; DNA: Deoxyribonucleic Acid; ESSENCE: Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations; HPA axis: Hypothalamic-Pituitary-Adrenal Axis; IQ: Intelligence Quotient; LoF: Loss-of-Function; MAPP: Maltreatment-Associated Psychiatric Problems; OCD: Obsessive Compulsive Disorder; PTSD: Post Traumatic Stress Disorder; QoL: Quality of Life; RNA: Ribonucleic Acid (RNA); SNP: Single-Nucleotide Polymorphism; WGS: Whole-Genome Sequencing;
Acknowledgment

The author is very grateful to all the children, adolescents and their families who across the past years have shared their experiences as part of my clinical practice. Their experiences have inspired my theoretical research, thereby contributing to the development of the dynamic model, including the hypotheses guiding the model.

Conflict of interest

The author declares no conflicts of interest.

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