Astrocytes in Down Syndrome Across the Lifespan

Ponroy Bally, Blandine and Murai, Keith K. (2021) Astrocytes in Down Syndrome Across the Lifespan. Frontiers in Cellular Neuroscience, 15. ISSN 1662-5102

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Abstract

Down Syndrome (DS) is the most common genetic cause of intellectual disability in which delays and impairments in brain development and function lead to neurological and cognitive phenotypes. Traditionally, a neurocentric approach, focusing on neurons and their connectivity, has been applied to understanding the mechanisms involved in DS brain pathophysiology with an emphasis on how triplication of chromosome 21 leads to alterations in neuronal survival and homeostasis, synaptogenesis, brain circuit development, and neurodegeneration. However, recent studies have drawn attention to the role of non-neuronal cells, especially astrocytes, in DS. Astrocytes comprise a large proportion of cells in the central nervous system (CNS) and are critical for brain development, homeostasis, and function. As triplication of chromosome 21 occurs in all cells in DS (with the exception of mosaic DS), a deeper understanding of the impact of trisomy 21 on astrocytes in DS pathophysiology is warranted and will likely be necessary for determining how specific brain alterations and neurological phenotypes emerge and progress in DS. Here, we review the current understanding of the role of astrocytes in DS, and discuss how specific perturbations in this cell type can impact the brain across the lifespan from early brain development to adult stages. Finally, we highlight how targeting, modifying, and/or correcting specific molecular pathways and properties of astrocytes in DS may provide an effective therapeutic direction given the important role of astrocytes in regulating brain development and function.

Item Type: Article
Subjects: OA Open Library > Medical Science
Depositing User: Unnamed user with email support@oaopenlibrary.com
Date Deposited: 13 Apr 2023 06:48
Last Modified: 16 Sep 2023 04:59
URI: http://archive.sdpublishers.com/id/eprint/500

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