miR155, triplicated in Down syndrome, regulates the development of neural stem cells and GABAergic interneurons in Alzheimer's disease mouse and human iPSC models
Xiaodong Zhu, Jean‐Vianney Haure‐Mirande, Mesude Bicak, Pengfei Dong, Ilya Kruglikov, Aiqun Li, Aisha Al‐subaie, Valentina Fossati, Scott Noggle, Sam Gandy, Michelle E. Ehrlich · 2026
Read miR155, triplicated in Down syndrome, regulates the development of neural stem cells and GABAergic interneurons in Alzheimer's disease mouse and human iPSC models by Xiaodong Zhu, Jean‐Vianney Haure‐Mirande, Mesude Bicak, Pengfei Dong, Ilya Kruglikov, Aiqun Li, Aisha Al‐subaie, Valentina Fossati, Scott Noggle, Sam Gandy, Michelle E. Ehrlich (2026) in the Tower of Babel, a free online library of public-domain works preserved in clean, searchable text. No sign-up. The full text is served as a plain-text file at a predictable URL, where text is present: https://antarctic-labs.com/tower-of-babel/PMC13452021.txt.
Description
Zhu and colleagues study a small RNA that is overproduced in both Down syndrome and Alzheimer's disease in this 2026 paper. The RNA, miR155, sits on chromosome 21, so people with Down syndrome carry an extra copy, and it is also elevated in Alzheimer's brains. The team worked with human stem-cell-derived brain cells. They also used cortical organoids and Alzheimer's model mice. They deleted or boosted miR155 to see what it does in neurons.
Deleting miR155 made neural stem cells multiply more and generate more GABAergic interneurons, the brain's main inhibitory cells, while boosting it had the opposite effect. In mice, deletion likewise expanded the hippocampal stem cell pool and increased those interneurons. The authors suggest miR155, already known for driving inflammation in immune cells, also shapes brain development and could be a treatment target.
Catalog record
| CREATOR | Xiaodong Zhu, Jean‐Vianney Haure‐Mirande, Mesude Bicak, Pengfei Dong, Ilya Kruglikov, Aiqun Li, Aisha Al‐subaie, Valentina Fossati, Scott Noggle, Sam Gandy, Michelle E. Ehrlich |
|---|---|
| YEAR | 2026 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 85 KB |
| LICENSE | https://creativecommons.org/licenses/by/4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |