Reversing Pathophysiology in Fragile X Syndrome Mice by Promoting PGC-1α and Mitochondrial Functions
KO mice. Together, our findings identify AMPK-CREB signaling and PGC-1α as promising and selective therapeutic targets for FXS and reveal the broad impact of restoring PGC-1α on FXS pathophysiology. One Sentence Summary: Promoting PGC-1α Reverses FXS Pathophysiology.
Authors
- Nien‐Pei Tsai (ORCID: https://orcid.org/0000-0003-1032-0107)
- Austin Cyphersmith
- Kwan Young Lee (ORCID: https://orcid.org/0000-0003-2890-0580)
- Justin S. Rhodes (ORCID: https://orcid.org/0000-0002-4871-4331)
- Vipendra Kumar (ORCID: https://orcid.org/0009-0006-3656-0837)
- Kingsley A. Boateng (ORCID: https://orcid.org/0000-0002-1974-5905)
- Matthew S Babik
- Gaurav Goswami
- Anirudh Acharya
Institutions
- University of Illinois Urbana-Champaign (US)
- Institute for Stem Cell Biology and Regenerative Medicine (IN)
Publication Details
- Journal
- bioRxiv (Cold Spring Harbor Laboratory)
- Published
- 2026-04-15
- DOI
- https://doi.org/10.64898/2026.04.13.718178
- Primary Topic
- Genetics and Neurodevelopmental Disorders
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- FRAXA Research Foundation
- National Institute of Mental Health
- National Institute of Neurological Disorders and Stroke