A new study by researchers at the Azrieli Centre for Autism Research (ACAR) has uncovered a promising approach for reducing brain inflammation.听
Glial cells, which support and protect neurons, can become overactive during injury and brain inflammation. This overactivity may contribute to chronic neurodegeneration and worsen brain disorders. Understanding how this process, called reactive gliosis, is controlled could help scientists better understand brain diseases and improve treatments.听听
The study, , found that removing a gene linked to autism, CHD8, from certain brain cells called astrocytes, reduces over-reactivity during brain injury and inflammations in experimental mouse models.听
Researchers found that adult mice with the CHD8 gene removed from astrocytes experienced less brain inflammation and alleviated symptoms compared to mice with the gene. Removing the gene changed how DNA is packaged and transcribed in astrocytes, leading to changes in the activity of other genes necessary for the growth and communication of these brain cells with others.听
The team was eager to explore how their discovery could be applied in real-world treatments. Further work showed they could reduce astrocyte reactivity directly in the brain using CRISPR, a specific gene-editing technology that is revolutionizing biomedical research. These results suggest that targeting the CHD8 gene in astrocytes in the adult brain could be a promising approach for reducing brain inflammation and treating related brain disorders.听听
This study was led by Platon Megagiannis, a PhD student in the Integrated Program in Neuroscience of 看片视频 University, in the lab of Yang Zhou. Contributing labs include those of Guy Rouleau, Stefano Stifani, and Keith Murai from ACAR; Neville Sanjana from the New York Genome Center; Gene Yeo and Trey Ideker from the University of California San Diego; and Guoping Feng at MIT.
Read the research paper
Autism-associated CHD8 controls reactive gliosis and neuroinflammation via remodeling chromatin in astrocytes.听Megagiannis, Platon et al.听Cell Reports, Volume 43, Issue 8, 114637.听DOI:
Yang Zhou (left) and Platon听Megagiannis.
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