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Cross-species models of attention-deficit/hyperactivity disorder and autism spectrum disorder: Lessons from CNTNAP2, ADGRL3, and PARK2

Vecchia E. D., Mortimer N., Palladino V. S., Kittel-Schneider S., Lesh K. Yu., Reif A., Schenck A., Norton W. H. J.
Psychiatric Genetics
Vol.29, Issue1, P. 1-17
Опубликовано: 2019
Тип ресурса: Статья

DOI:10.1097/YPG.0000000000000211

Аннотация:
Animal and cellular models are essential tools for all areas of biological research including neuroscience. Model systems can also be used to investigate the pathophysiology of psychiatric disorders such as attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). In this review, we provide a summary of animal and cellular models for three genes linked to ADHD and ASD in human patients - CNTNAP2, ADGRL3, and PARK2. We also highlight the strengths and weaknesses of each model system. By bringing together behavioral and neurobiological data, we demonstrate how a crossspecies approach can provide integrated insights into gene function and the pathogenesis of ADHD and ASD. The knowledge gained from transgenic models will be essential to discover and validate new treatment targets for these disorders. Copyright © 2018 The Author(s).
Ключевые слова:
ADGRL3; attention-deficit/hyperactivity disorder; autism spectrum disorder; CNTNAP2; cross-species; Drosophila; human induced pluripotent stem cells; mouse; PARK2; zebrafish
adgrl3 gene; Article; attention deficit disorder; autism; cntnap2 gene; Drosophila melanogaster; DSM-5; environmental factor; gene; genetic variability; heredity; human; induced pluripotent stem cell; mouse; neuropathology; nonhuman; park2 gene; penetrance; priority journal; transgenic organism; zebra fish; animal; attention deficit disorder; autism; biological model; disease model; Drosophila; metabolism; pathophysiology; CNTNAP2 protein, human; G protein coupled receptor; membrane protein; nerve protein; parkin; ubiquitin protein ligase; Animals; Attention Deficit Disorder with Hyperactivity; Autism Spectrum Disorder; Disease Models, Animal; Drosophila; Humans; Membrane Proteins; Mice; Models, Biological; Nerve Tissue Proteins; Receptors, G-Protein-Coupled; Ubiquitin-Protein Ligases; Zebrafish
Язык текста: Английский
ISSN: 1473-5873
Vecchia E. D.
Mortimer N.
Palladino V. S.
Kittel-Schneider S.
Lesh K. Yu. Klaus-Peter Yulius 1957-
Reif A.
Schenck A.
Norton W. H. J.
Веcчиа Е. Д.
Мортимер Н.
Палладино В. С.
Киттел-Счнеидер С.
Леш К. Ю. Клаус-Петер Юлиус 1957-
Реиф А.
Сченcк А.
Нортон W. Х. Й.
Cross-species models of attention-deficit/hyperactivity disorder and autism spectrum disorder: Lessons from CNTNAP2, ADGRL3, and PARK2
Текст визуальный непосредственный
Psychiatric Genetics
Lippincott Williams & Wilkins
Vol.29, Issue1 P. 1-17
2019
Статья
ADGRL3 attention-deficit/hyperactivity disorder autism spectrum disorder CNTNAP2 cross-species Drosophila human induced pluripotent stem cells mouse PARK2 zebrafish
adgrl3 gene Article attention deficit disorder autism cntnap2 gene Drosophila melanogaster DSM-5 environmental factor gene genetic variability heredity human induced pluripotent stem cell mouse neuropathology nonhuman park2 gene penetrance priority journal transgenic organism zebra fish animal attention deficit disorder autism biological model disease model Drosophila metabolism pathophysiology CNTNAP2 protein, human G protein coupled receptor membrane protein nerve protein parkin ubiquitin protein ligase Animals Attention Deficit Disorder with Hyperactivity Autism Spectrum Disorder Disease Models, Animal Drosophila Humans Membrane Proteins Mice Models, Biological Nerve Tissue Proteins Receptors, G-Protein-Coupled Ubiquitin-Protein Ligases Zebrafish
Animal and cellular models are essential tools for all areas of biological research including neuroscience. Model systems can also be used to investigate the pathophysiology of psychiatric disorders such as attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). In this review, we provide a summary of animal and cellular models for three genes linked to ADHD and ASD in human patients - CNTNAP2, ADGRL3, and PARK2. We also highlight the strengths and weaknesses of each model system. By bringing together behavioral and neurobiological data, we demonstrate how a crossspecies approach can provide integrated insights into gene function and the pathogenesis of ADHD and ASD. The knowledge gained from transgenic models will be essential to discover and validate new treatment targets for these disorders. Copyright © 2018 The Author(s).