Pridopidine Protects ALS Patient-Derived Neural Progenitor Cells via Sigma-1 Receptor Activation
expression and caspase-3 activation, and improved survival of ALS-NPCs under ER stress. Co-treatment with the selective S1R antagonist, NE-100, attenuated these effects, supporting an S1R-mediated mechanism of action for pridopidine. Together, these results demonstrate that S1R activation by pridopidine mitigates ER-stress-induced mitochondrial dysfunction and cell loss in ALS-NPCs, resulting in enhanced survival of NPCs supporting the therapeutic potential of pridopidine in ALS.
Authors
- May Meltzer
- Andrew M. Tan (ORCID: https://orcid.org/0000-0002-0099-8814)
- Noam Tzuri
- Michal Geva (ORCID: https://orcid.org/0000-0002-6949-0963)
- M. E. Hayden
- Rachel G. Lichtenstein (ORCID: https://orcid.org/0000-0002-2225-1068)
- Maya Shefler Zamir (ORCID: https://orcid.org/0009-0004-4828-0811)
Institutions
- Ben-Gurion University of the Negev (IL)
- University of British Columbia (CA)
- Yale University (US)
- Unilever (Netherlands) (NL)
Publication Details
- Journal
- International Journal of Molecular Sciences
- Published
- 2026-04-14
- DOI
- https://doi.org/10.3390/ijms27083489
- Primary Topic
- Pharmacological Receptor Mechanisms and Effects
- Type
- article
- Field-Weighted Citation Impact
- 0.00