Genetic Ablation of <i>Sarm1</i> Mitigates Disease Acceleration after Traumatic Brain Injury in the <scp>SOD1<sup>G93A</sup></scp> Transgenic Mouse Model of Amyotrophic Lateral Sclerosis
SARM1-mediated axonal death pathway promotes pathogenesis after TBI in SOD1<sup>G93A</sup> mice suggesting that anti-SARM1 therapeutics are a viable approach to preserve neurological function in injury-accelerated G93A-SOD1 ALS. ANN NEUROL 2025;97:963-975.
Authors
- Robert H. Brown (ORCID: https://orcid.org/0000-0001-6062-1528)
- James Bouley
- Nils Henninger (ORCID: https://orcid.org/0000-0002-3883-5623)
- Stefano Simonini (ORCID: https://orcid.org/0000-0002-8563-0129)
- Alexandra Weiss (ORCID: https://orcid.org/0000-0003-0169-6591)
- Elif O. Dogan
Institutions
- University of Massachusetts Chan Medical School (US)
Publication Details
- Journal
- Annals of Neurology
- Published
- 2025-01-10
- DOI
- https://doi.org/10.1002/ana.27174
- Citations
- 3
- Primary Topic
- Amyotrophic Lateral Sclerosis Research
- Type
- article
- Field-Weighted Citation Impact
- 4.17
Funders
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke