This poster presents Ncardia’s human iPSC-derived motor neuron platform for amyotrophic lateral sclerosis (ALS) research, using a CRISPR-engineered TDP-43 mutation to model key disease-associated phenotypes. The platform combines high-content imaging, molecular analysis and electrophysiological measurements to support the evaluation of potential ALS therapeutics.
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How TDP-43 mislocalisation and pathological aggregation are quantified in human iPSC-derived motor neurons using high-content imaging
How STMN2 protein reduction and abnormal STMN2 splicing provide measurable readouts of ALS-related molecular pathology
How multi-electrode array (MEA) recordings and neurofilament-L measurements capture changes in neuronal activity and disease-associated phenotypes
How 384-well miniaturised assays support compound screening, alongside proof-of-concept gene therapy experiments demonstrating a reduction in TDP-43 aggregation