Amandeep Girdhar

The paper engineers chimeric proteins to replace ALS-causing FUS and TDP-43, improving neuronal health by reducing aggregation and restoring nuclear functions.

This study develops a human neuronal model with the TDP-43 A315T mutation to study ALS-related protein dysfunction and therapeutic responses.

This study shows that Kapβ2 protein interacts with poly(GR) and reduces its neurotoxicity in C9orf72-linked ALS/FTD by improving neuron survival.

The paper investigates the role of CNC1 gene in TDP-43 aggregation-induced oxidative stress-mediated cell death in a yeast model of ALS, finding that CNC1 deletion reduces TDP-43 toxicity.

This study uses computational methods to identify AIM4's binding site on TDP-43 and shows it inhibits LLPS of a TDP-43 mutant in vitro.