Shashirekha S. Markandaiah

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

CAR-T cells targeting uPAR selectively ablate pathogenic microglia while sparing neurons, enabling precision immunotherapy for ALS.

This study shows glucose hypometabolism in C9orf72-related ALS/FTD leads to DPR production, neuronal death, and motor dysfunction through GCN2 activation.

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

This study shows that C9orf72 poly(PR) causes nucleolar stress and neurotoxicity, which can be mitigated by reducing p53 levels in fly and rat models.

This study shows that reducing ephrinB2 in spinal cord astrocytes of ALS mice preserves diaphragm innervation and respiratory function.