For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
0
views
69
references
 Top references
cited by
0
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      1,088
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Genetic Modifications of Developmental Dyslexia and Its Representation Using In Vivo, In Vitro Model

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Dyslexia is a genetic and heritable disorder that has yet to discover the treatment of it, especially at the molecular and drug intervention levels. This review provides an overview of the current findings on the environmental and genetic factors involved in developmental dyslexia. The latest techniques used in diagnosing the disease and macromolecular factors findings may contribute to a higher degree of development in detangling the proper management and treatment for dyslexic individuals. Furthermore, this review tried to put together all the models used in the current dyslexia research for references in future studies that include animal models as well as in vitro models and how the previous research has provided consistent data across many years and regions. Thus, we suggest furthering the studies using an organoid model based on the existing gene polymorphism, pathways, and neuronal function input.

          Related collections

          Most cited references69

          • Record: found
          • Abstract: found
          • Article: not found

          Developmental dyslexia.

          Robin L Peterson, Bruce F. Pennington (2015)
          This review uses a levels-of-analysis framework to summarize the current understanding of developmental dyslexia's etiology, brain bases, neuropsychology, and social context. Dyslexia is caused by multiple genetic and environmental risk factors as well as their interplay. Several candidate genes have been identified in the past decade. At the brain level, dyslexia is associated with aberrant structure and function, particularly in left hemisphere reading/language networks. The neurocognitive influences on dyslexia are also multifactorial and involve phonological processing deficits as well as weaknesses in other oral language skills and processing speed. We address contextual issues such as how dyslexia manifests across languages and social classes as well as what treatments are best supported. Throughout the review, we highlight exciting new research that cuts across levels of analysis. Such work promises eventually to provide a comprehensive explanation of the disorder as well as its prevention and remediation.
          Article 0 comments Cited 104 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Developmental dyslexia.

            Jean-François Demonet, Mark Taylor, Yves Chaix (2004)
            Developmental dyslexia, or specific reading disability, is a disorder in which children with normal intelligence and sensory abilities show learning deficits for reading. Substantial evidence has established its biological origin and the preponderance of phonological disorders even though important phenotypic variability and comorbidity have been recorded. Diverse theories have been proposed to account for the cognitive and neurological aspects of dyslexia. Findings of genetic studies show that different loci affect specific reading disability although a direct relation has not been established between symptoms and a given genomic locus. In both children and adults with dyslexia, results of neuroimaging studies suggest defective activity and abnormal connectivity between regions crucial for language functions--eg, the left fusiform gyrus for reading--and changes in brain activity associated with performance improvement after various remedial interventions.
            Article 0 comments Cited 98 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Robo1 regulates the development of major axon tracts and interneuron migration in the forebrain.

              Céline Plachez, L Camurri, Alexander L. Richards … (2006)
              The Slit genes encode secreted ligands that regulate axon branching, commissural axon pathfinding and neuronal migration. The principal identified receptor for Slit is Robo (Roundabout in Drosophila). To investigate Slit signalling in forebrain development, we generated Robo1 knockout mice by targeted deletion of exon 5 of the Robo1 gene. Homozygote knockout mice died at birth, but prenatally displayed major defects in axon pathfinding and cortical interneuron migration. Axon pathfinding defects included dysgenesis of the corpus callosum and hippocampal commissure, and abnormalities in corticothalamic and thalamocortical targeting. Slit2 and Slit1/2 double mutants display malformations in callosal development, and in corticothalamic and thalamocortical targeting, as well as optic tract defects. In these animals, corticothalamic axons form large fasciculated bundles that aberrantly cross the midline at the level of the hippocampal and anterior commissures, and more caudally at the medial preoptic area. Such phenotypes of corticothalamic targeting were not observed in Robo1 knockout mice but, instead, both corticothalamic and thalamocortical axons aberrantly arrived at their respective targets at least 1 day earlier than controls. By contrast, in Slit mutants, fewer thalamic axons actually arrive in the cortex during development. Finally, significantly more interneurons (up to twice as many at E12.5 and E15.5) migrated into the cortex of Robo1 knockout mice, particularly in both rostral and parietal regions, but not caudal cortex. These results indicate that Robo1 mutants have distinct phenotypes, some of which are different from those described in Slit mutants, suggesting that additional ligands, receptors or receptor partners are likely to be involved in Slit/Robo signalling.
              Article 0 comments Cited 78 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (nlm-ta): Glob Med Genet
                Journal ID (iso-abbrev): Glob Med Genet
                Journal ID (doi): 10.1055/s-00046370
                Title: Global Medical Genetics
                Publisher: Georg Thieme Verlag KG (Rüdigerstraße 14, 70469 Stuttgart, Germany )
                ISSN (Electronic): 2699-9404
                Publication date (Electronic): 27 February 2024
                Publication date Collection: January 2024
                Publication date PMC-release: 1 February 2024
                Volume: 11
                Issue: 1
                Pages: 76-85
                Affiliations
                [1 ]Department of Neurosciences, School of Medical Sciences, Universiti Sains Malaysia, Kelantan, Malaysia
                [2 ]Department of Electronic Engineering, Faculty of Engineering and Green Technology, Universiti Tunku Abdul Rahman, Kampar, Perak, Malaysia
                [3 ]Centre for Healthcare Science and Technology, Universiti Tunku Abdul Rahman, Kampar, Perak, Malaysia
                [4 ]Faculty of Medicine, Universiti Sultan Zainal Abidin, Terengganu, Malaysia
                [5 ]Department of Biochemistry, Faculty of Medicine, Manipal University College Malaysia, Melaka, Malaysia
                Author notes
                Address for correspondence Faidruz A. Jam, PhD Manipal University College Malaysia Jalan Padang Jambu, Bukit Baru, 75150 MelakaMalaysia faidruz.jam@ 123456manipal.edu.my
                Article
                Publisher ID: GMG-D-24-00006
                DOI: 10.1055/s-0044-1781456
                PMC ID: 10898997
                PubMed ID: 38414980
                SO-VID: a43d5170-47e6-4f24-9053-7aab6afab489
                Copyright © The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. ( https://creativecommons.org/licenses/by/4.0/ )
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Funding
                Funding None.
                Categories
                Subject: Review Article

                Keywords: dyslexia,genetic of language disorder,developmental disorder
                Data availability:
                Keywords: dyslexia, genetic of language disorder, developmental disorder

                Comments

                Comment on this article