This poster presents Ncardia’s human iPSC-based platform for modeling and screening amyotrophic lateral sclerosis, built around disease-relevant motor neuron assays that capture key pathological hallmarks of TDP-43 dysfunction.
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How CRISPR-engineered TDP-43 mutant motor neurons reproduce core ALS phenotypes, including TDP-43 mislocalization, aggregation, STMN2 reduction and mis-splicing.
High-content imaging and miniaturized assay formats that enable quantitative, scalable assessment of protein aggregation and molecular rescue.
Electrophysiological characterization by MEA, demonstrating altered network activity and functional deficits in mutant motor neurons.
Proof-of-concept data showing successful transduction and therapeutic rescue, including significant reduction of TDP-43 aggregation and improvement of functional readouts.
Why integrating molecular, imaging, and functional endpoints in a single human-relevant platform supports more predictive evaluation of ALS therapeutic candidates.