Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Jun 23:14:877928.
doi: 10.3389/fnsyn.2022.877928. eCollection 2022.

Astrocyte: A Foe or a Friend in Intellectual Disability-Related Diseases

Busong Wang  1 , Lu Zou  1 , Min Li  1 , Liang Zhou  1
Affiliations
Review

Astrocyte: A Foe or a Friend in Intellectual Disability-Related Diseases

Busong Wang et al. Front Synaptic Neurosci. .

Abstract

Intellectual disabilities are a type of neurodevelopmental disease caused by neurological dysfunction. Their incidence is largely associated with neural development. Astrocytes are the most widely distributed cells in the mammalian brain. Previous studies have reported that astrocytes only supported and separated the neurons in the brain. However, recent studies have found that they also play an important role in neural development. Understanding the astrocyte mechanism in intellectual development disorder-related diseases will help provide new therapeutic targets for the treatment of intellectual disability-related diseases. This mini-review introduced the association between astrocyte and intellectual disabilities. Furthermore, recent advances in genetic and environmental factors causing intellectual disability and different pharmaceutical effects of intellectual disability-related drugs on astrocytes have been summarised. Finally, we discussed future perspectives of astrocyte-based therapy for intellectual disability.

Keywords: astrocyte; central nervous system; drug therapy; intellectual disability; neurodevelopment.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Similar articles

See all similar articles

Cited by

References

    1. Abdelhak A., Foschi M., Abu-Rumeileh S., Yue J. K., D’Anna L., Huss A., et al. (2022). Blood GFAP as an emerging biomarker in brain and spinal cord disorders. Nat. Rev. Neurol. 18 158–172. 10.1038/s41582-021-00616-613 - DOI - PubMed
    1. Andoh-Noda T., Akamatsu W., Miyake K., Matsumoto T., Yamaguchi R., Sanosaka T., et al. (2015). Differentiation of multipotent neural stem cells derived from Rett syndrome patients is biased toward the astrocytic lineage. Mol. Brain 8:31. 10.1186/s13041-015-0121-122 - DOI - PMC - PubMed
    1. Araujo B. H. S., Kaid C., De Souza J. S., Gomes, da Silva S., Goulart E., et al. (2018). Down syndrome iPSC-derived astrocytes impair neuronal synaptogenesis and the mTOR pathway in vitro. Mol. Neurobiol. 55 5962–5975. 10.1007/s12035-017-0818-816 - DOI - PubMed
    1. Arena A., Iyer M. A., Milenkovic I., Kovacs G. G., Ferrer I., Perluigi M., et al. (2017). Developmental expression and dysregulation of miR-146a and miR-155 in Down’s syndrome and mouse models of Down’s syndrome and Alzheimer’s disease. Curr. Alzheimer Res. 14 1305–1317. 10.2174/1567205014666170706112701 - DOI - PubMed
    1. Aureli M., Mauri L., Ciampa M. G., Prinetti A., Toffano G., Secchieri C., et al. (2016). GM1 ganglioside: past studies and future potential. Mol. Neurobiol. 53 1824–1842. 10.1007/s12035-015-9136-z - DOI - PubMed

LinkOut - more resources