Fen‐Biao Gao

This study shows that elevating neuronal CYLD causes FTD-like behavioral and physiological deficits in mice, with M719V mutation acting as a gain-of-function.

This study shows NLK disrupts nuclear import, causing TDP43 mislocalization in ALS, and suggests NLK as a therapeutic target.

This study shows that C9orf72 ALS patient motor neurons are more vulnerable to trauma, with TDP-43 mislocalization and reduced recovery after repeated mild injuries.

The paper identifies AUG initiation codons for antisense DPRs in C9ORF72-ALS/FTD, showing redundancy in start codon usage and distinct translation factors for sense and antisense transcripts.

This study removes a hexanucleotide repeat expansion in C9ORF72 using CRISPR/Cas9 in cell and animal models, reducing disease hallmarks.

This study uses C. elegans models to show that eIF2D is essential for RAN translation in C9orf72 expansions, and its inhibition extends lifespan and reduces disease.

This study examines C9orf72 ALS/FTD patient-derived iPSC-microglia mono-cultures, finding they form RNA foci, have reduced C9orf72 protein, and show endosomal-lysosomal dysfunction, but no significant microglial-enriched gene expression differences.