Aaron R. Haeusler

This paper delivers (G4C2)149 repeats intrathecally in C9orf72-deficient mice, revealing mild motor dysfunction and ALS/FTD pathological features.

This study identifies RNA G-quadruplexes as tunable regulators of FUS phase separation, showing they can inhibit or nucleate aggregation depending on structure and concentration.

This study shows that increased neuronal activity can restore circadian function in Drosophila models of C9orf72-ALS/FTD.

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

This study shows that C9orf72 repeat expansion neurons have altered transcriptomes under different stimulation conditions, revealing activity-dependent gene dysregulation in ALS/FTD.

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 astrocytic expression of mutant FUS causes TNF-dependent neurodegeneration in ALS, highlighting a therapeutic target.