<i>Dyrk1a</i> from Gene Function in Development and Physiology to Dosage Correction across Life Span in Down Syndrome

Down syndrome is the main cause of intellectual disabilities with a large set of comorbidities from developmental origins but also that appeared across life span. Investigation of the genetic overdosage found in Down syndrome, due to the trisomy of human chromosome 21, has pointed to one main driver...

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Autores principales:	Helin Atas-Ozcan, Véronique Brault, Arnaud Duchon, Yann Herault
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	trisomy 21 neurodevelopmental disorder mouse model cognition learning and memory preclinical trial Genetics QH426-470
Acceso en línea:	https://doaj.org/article/b119098bae63424dbbd3a1627c889041
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spelling	oai:doaj.org-article:b119098bae63424dbbd3a1627c8890412021-11-25T17:42:31Z<i>Dyrk1a</i> from Gene Function in Development and Physiology to Dosage Correction across Life Span in Down Syndrome10.3390/genes121118332073-4425https://doaj.org/article/b119098bae63424dbbd3a1627c8890412021-11-01T00:00:00Zhttps://www.mdpi.com/2073-4425/12/11/1833https://doaj.org/toc/2073-4425Down syndrome is the main cause of intellectual disabilities with a large set of comorbidities from developmental origins but also that appeared across life span. Investigation of the genetic overdosage found in Down syndrome, due to the trisomy of human chromosome 21, has pointed to one main driver gene, the <i>Dual-specificity tyrosine-regulated kinase 1A (Dyrk1a).</i> Dyrk1a is a murine homolog of the drosophila <i>minibrain</i> gene. It has been found to be involved in many biological processes during development and in adulthood. Further analysis showed its haploinsufficiency in mental retardation disease 7 and its involvement in Alzheimer’s disease. DYRK1A plays a role in major developmental steps of brain development, controlling the proliferation of neural progenitors, the migration of neurons, their dendritogenesis and the function of the synapse. Several strategies targeting the overdosage of DYRK1A in DS with specific kinase inhibitors have showed promising evidence that DS cognitive conditions can be alleviated. Nevertheless, providing conditions for proper temporal treatment and to tackle the neurodevelopmental and the neurodegenerative aspects of DS across life span is still an open question.Helin Atas-OzcanVéronique BraultArnaud DuchonYann HeraultMDPI AGarticletrisomy 21neurodevelopmental disordermouse modelcognitionlearning and memorypreclinical trialGeneticsQH426-470ENGenes, Vol 12, Iss 1833, p 1833 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	trisomy 21 neurodevelopmental disorder mouse model cognition learning and memory preclinical trial Genetics QH426-470
spellingShingle	trisomy 21 neurodevelopmental disorder mouse model cognition learning and memory preclinical trial Genetics QH426-470 Helin Atas-Ozcan Véronique Brault Arnaud Duchon Yann Herault <i>Dyrk1a</i> from Gene Function in Development and Physiology to Dosage Correction across Life Span in Down Syndrome
description	Down syndrome is the main cause of intellectual disabilities with a large set of comorbidities from developmental origins but also that appeared across life span. Investigation of the genetic overdosage found in Down syndrome, due to the trisomy of human chromosome 21, has pointed to one main driver gene, the <i>Dual-specificity tyrosine-regulated kinase 1A (Dyrk1a).</i> Dyrk1a is a murine homolog of the drosophila <i>minibrain</i> gene. It has been found to be involved in many biological processes during development and in adulthood. Further analysis showed its haploinsufficiency in mental retardation disease 7 and its involvement in Alzheimer’s disease. DYRK1A plays a role in major developmental steps of brain development, controlling the proliferation of neural progenitors, the migration of neurons, their dendritogenesis and the function of the synapse. Several strategies targeting the overdosage of DYRK1A in DS with specific kinase inhibitors have showed promising evidence that DS cognitive conditions can be alleviated. Nevertheless, providing conditions for proper temporal treatment and to tackle the neurodevelopmental and the neurodegenerative aspects of DS across life span is still an open question.
format	article
author	Helin Atas-Ozcan Véronique Brault Arnaud Duchon Yann Herault
author_facet	Helin Atas-Ozcan Véronique Brault Arnaud Duchon Yann Herault
author_sort	Helin Atas-Ozcan
title	<i>Dyrk1a</i> from Gene Function in Development and Physiology to Dosage Correction across Life Span in Down Syndrome
title_short	<i>Dyrk1a</i> from Gene Function in Development and Physiology to Dosage Correction across Life Span in Down Syndrome
title_full	<i>Dyrk1a</i> from Gene Function in Development and Physiology to Dosage Correction across Life Span in Down Syndrome
title_fullStr	<i>Dyrk1a</i> from Gene Function in Development and Physiology to Dosage Correction across Life Span in Down Syndrome
title_full_unstemmed	<i>Dyrk1a</i> from Gene Function in Development and Physiology to Dosage Correction across Life Span in Down Syndrome
title_sort	<i>dyrk1a</i> from gene function in development and physiology to dosage correction across life span in down syndrome
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/b119098bae63424dbbd3a1627c889041
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<i>Dyrk1a</i> from Gene Function in Development and Physiology to Dosage Correction across Life Span in Down Syndrome

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