We’re proud to share that Synapticure’s R&D lab contributed to a new study from Dr. Sami Barmada’s group at the University of Michigan, published in the Journal of Clinical Investigation. This important work uncovers how a disrupted protein, Nemo-like kinase (NLK), leads to a central hallmark of ALS biology. We are excited to have played a part in this paper. Using our granulin-deficient 3D cortical brain spheroids, a system with these central hallmarks of ALS and FTD biology, Synapticure validated that this protein is elevated consistent with what’s observed in patient tissue. This study highlights the power of our patient-derived brain model platform to: - Recapitulate human disease biology - Validate therapeutic targets emerging from discovery pipelines - Provide a translational bridge between patient data and preclinical development Congratulations to Dr. Barmada, Michael Bekier, Emile Pinarbasi, and all of the authors on this important advance. We’re excited to see our models helping accelerate insights that move the field closer to effective therapies for ALS and related neurodegenerative diseases.
Neuroscience Ph.D. | Director of Disease Modeling @ Synapticure | neurodegeneration to translation | early-stage biotech builder
Awesome new paper from Sami Barmada's lab at UMich, whose team continues to push the field forward in unraveling ALS. This work elucidates the role of nemo-like kinase (NLK) in regulating nucleocytoplasmic transport, and shows that elevated NLK directly contributes to TDP-43 mislocalization, emphasizing NLK’s importance as both a driver of disease and promising therapeutic target. The Synapticure lab team and I were glad to contribute to this study using our granulin-deficient 3D brain spheroids, where we observed elevated NLK levels consistent with patient tissue. Congratulations to Sami, Michael, Emile, and the full team on this important advance in ALS research! https://lnkd.in/e-9AaZXP
