Potential role of JAK-STAT signaling pathway in the neurogenic-to-gliogenic shift in down syndrome brain
Trisomy of human chromosome 21 in Down syndrome (DS) leads to several phenotypes, such as mild-to-severe intellectual disability, hypotonia, and craniofacial dysmorphisms. These are fundamental hallmarks of the disorder that affect the quality of life of most individuals with DS. Proper brain develo...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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Hindawi Publishing Corporation
2016
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| Online Access: | http://psasir.upm.edu.my/id/eprint/23186/1/23186.pdf |
| _version_ | 1825925303399088128 |
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| author | Lee, Han Chung Tan, Kai Leng Cheah, Pike See Ling, King Hwa |
| author_facet | Lee, Han Chung Tan, Kai Leng Cheah, Pike See Ling, King Hwa |
| author_sort | Lee, Han Chung |
| collection | UPM |
| description | Trisomy of human chromosome 21 in Down syndrome (DS) leads to several phenotypes, such as mild-to-severe intellectual disability, hypotonia, and craniofacial dysmorphisms. These are fundamental hallmarks of the disorder that affect the quality of life of most individuals with DS. Proper brain development involves meticulous regulation of various signaling pathways, and dysregulation may result in abnormal neurodevelopment. DS brain is characterized by an increased number of astrocytes with reduced number of neurons. In mouse models for DS, the pool of neural progenitor cells commits to glia rather than neuronal cell fate in the DS brain. However, the mechanism(s) and consequences of this slight neurogenic-to-gliogenic shift in DS brain are still poorly understood. To date, Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling has been proposed to be crucial in various developmental pathways, especially in promoting astrogliogenesis. Since both human and mouse models of DS brain exhibit less neurons and a higher percentage of cells with astrocytic phenotypes, understanding the role of JAK-STAT signaling in DS brain development will provide novel insight into its role in the pathogenesis of DS brain and may serve as a potential target for the development of effective therapy to improve DS cognition. |
| first_indexed | 2024-03-06T07:56:08Z |
| format | Article |
| id | upm.eprints-23186 |
| institution | Universiti Putra Malaysia |
| language | English |
| last_indexed | 2024-03-06T07:56:08Z |
| publishDate | 2016 |
| publisher | Hindawi Publishing Corporation |
| record_format | dspace |
| spelling | upm.eprints-231862016-06-10T09:05:38Z http://psasir.upm.edu.my/id/eprint/23186/ Potential role of JAK-STAT signaling pathway in the neurogenic-to-gliogenic shift in down syndrome brain Lee, Han Chung Tan, Kai Leng Cheah, Pike See Ling, King Hwa Trisomy of human chromosome 21 in Down syndrome (DS) leads to several phenotypes, such as mild-to-severe intellectual disability, hypotonia, and craniofacial dysmorphisms. These are fundamental hallmarks of the disorder that affect the quality of life of most individuals with DS. Proper brain development involves meticulous regulation of various signaling pathways, and dysregulation may result in abnormal neurodevelopment. DS brain is characterized by an increased number of astrocytes with reduced number of neurons. In mouse models for DS, the pool of neural progenitor cells commits to glia rather than neuronal cell fate in the DS brain. However, the mechanism(s) and consequences of this slight neurogenic-to-gliogenic shift in DS brain are still poorly understood. To date, Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling has been proposed to be crucial in various developmental pathways, especially in promoting astrogliogenesis. Since both human and mouse models of DS brain exhibit less neurons and a higher percentage of cells with astrocytic phenotypes, understanding the role of JAK-STAT signaling in DS brain development will provide novel insight into its role in the pathogenesis of DS brain and may serve as a potential target for the development of effective therapy to improve DS cognition. Hindawi Publishing Corporation 2016 Article PeerReviewed application/pdf en http://psasir.upm.edu.my/id/eprint/23186/1/23186.pdf Lee, Han Chung and Tan, Kai Leng and Cheah, Pike See and Ling, King Hwa (2016) Potential role of JAK-STAT signaling pathway in the neurogenic-to-gliogenic shift in down syndrome brain. Neural Plasticity, 2016. art. no. 7434191. pp. 1-12. ISSN 2090-5904; ESSN: 1687-5443 http://www.hindawi.com/journals/np/2016/7434191/abs/ 10.1155/2016/7434191 |
| spellingShingle | Lee, Han Chung Tan, Kai Leng Cheah, Pike See Ling, King Hwa Potential role of JAK-STAT signaling pathway in the neurogenic-to-gliogenic shift in down syndrome brain |
| title | Potential role of JAK-STAT signaling pathway in the neurogenic-to-gliogenic shift in down syndrome brain |
| title_full | Potential role of JAK-STAT signaling pathway in the neurogenic-to-gliogenic shift in down syndrome brain |
| title_fullStr | Potential role of JAK-STAT signaling pathway in the neurogenic-to-gliogenic shift in down syndrome brain |
| title_full_unstemmed | Potential role of JAK-STAT signaling pathway in the neurogenic-to-gliogenic shift in down syndrome brain |
| title_short | Potential role of JAK-STAT signaling pathway in the neurogenic-to-gliogenic shift in down syndrome brain |
| title_sort | potential role of jak stat signaling pathway in the neurogenic to gliogenic shift in down syndrome brain |
| url | http://psasir.upm.edu.my/id/eprint/23186/1/23186.pdf |
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