How brain cells restore healthy growth and connections after a disease-causing genetic deletion
Researchers at Virginia Tech have found that an experimental therapy using N-acetylcysteine (NAC) can help brain cells overcome damage caused by 22q11.2 deletion syndrome. The treatment works by reducing oxidative stress rather than repairing the genetic deletion itself.
Why it matters
This discovery offers a potential new pathway for treating genetic neurodevelopmental disorders by targeting cellular mechanisms instead of the underlying DNA.
edited by Lisa Lock , reviewed by Robert Egan
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Add as preferred source NAC therapy selectively circumvents oxidative stress-mediated restricted growth in 22q11-deleted L 2/3 PNs by engaging distinct cellular and transcriptional responses. Credit: Disease Models & Mechanisms (2026). DOI: 10.1242/dmm.052786 Scientists at Virginia Tech's Fralin Biomedical Research Institute at VTC have discovered how an experimental therapy can help brain cells overcome the effects of a disease-causing genetic deletion. Instead of repairing the deletion and its immediate consequences, the therapy redirects brain development by helping at-risk neurons grow and connect more normally.
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