Cell-type specific molecular and functional consequences of TDP-43 loss-of-function in human induced neurons

Read the publication to explore:

• The molecular consequences of TDP-43 knockdown using antisense oligonucleotides (ASOs) in hiPSC-derived glutamatergic and cholinergic motor neurons, including the mis-splicing of shared ALS-associated targets like STMN2 and UNC13A

• Electrophysiological findings revealing cell-type specific hyperexcitability, characterised by synchronised bursting in glutamatergic neurons versus asynchronous firing in motor neurons

• The expanded detection of cryptic splicing events, such as HDGFL2, when including astrocytes in the co-culture models

• How ioGlutamatergic Neurons and ioMotor Neurons were used