Investigating the pathogenesis of neurodegenerative diseases and developing new therapeutic approaches
The Mordes Lab investigates the mechanisms of neurodegeneration in ALS (amyotrophic lateral sclerosis), frontotemporal dementia (FTD), CTE, and Parkinson's disease (PD) with the goal of creating paths forward for the development of new targeted therapies. We integrate studies of patient brain samples with human stem cell-derived neurons and mouse models using transcriptomic and proteomic approaches as well as traditional immunostaining techniques. We are particularly interested in the role of selective autophagy in the maintenance of protein homeostasis in neurons. We also collaborate with the Prusiner lab to investigate the role of pathological alpha-synuclein in movement disorders. Please check out this site to learn more about our team, publications, and current research projects.
Human stem cell-derived excitatory neurons
NEWS
- May 2026: Julie presents our latest research on TBK1 and autophagy at the Target ALS Annual Meeting in Boston. Thank you Amy, Manish, and the entire TALS team.
- April 2026: Manuscript on TDP-43 Pathology in CTE with Dr. Thor Stein, Dr. Ann McKee, and colleagues in Boston is accepted.
- April 2026: Dan gives a research talk to the Packard Center for ALS Research investigator meeting.
- Feb 2026: Dan presents on TBK1-ALS/FTD models at the inaugural Gordon Research Conference on FTD. Thanks to Aimee and Fen-Biao for organizing.
- Jan 2026: Short article on the role of TBK1 in neurons is published in Autophagy.
- Dec 2025: Julie is awarded a Springboard Fellowship from Target ALS! This will accelerate her research on ALS and autophagy.
- Oct 2025: TBK1 and OPTN ALS/FTD proteomics study published in Cell Reports. Congrats to Julie, Lin, and team!
- July 2025: We welcome Sara to the lab, who's an expert on ALS and RNA biology.
Follow us on X: @MordesLab
The Mordes Lab values the uniqueness of everyone. We strive to uphold a safe, creative space for scientific collaboration and pursuit.
We welcome enthusiastic graduate students and post-doctoral fellows to join our group (see open positions)!
Example of iPSC-based modeling of neurodegenerative diseases. Disruption of protein homeostasis (via proteasome inhibition) is sufficient to induce mislocalization of the ALS-associated RNA-binding protein TDP-43 from the nucleus to the cytoplasm in the human pluripotent stem cell-derived motor neurons.
From (Nat Aging) DOI: 10.1038/s43587-024-00640-0.
Mordes Lab @ Weill Building for Neurosciences
1651 4th St., Mailroom 471A
San Francisco, CA, 94158, USA
(415) 353-1587