A. Nazlı Başak

This study shows that HTT CAA/CCA-loss variants increase toxicity in Huntington disease models independently of somatic repeat instability.

This study generates corticospinal-like neurons from SOX6+/NG2+ cortical progenitors using a multi-component transcriptional construct, achieving high fidelity in morphology, molecular, transcriptomic, and electrophysiological characteristics.

This study presents the crystal structure of human SOD1 and analyzes its structural dynamics and interactions with potential drug candidates for ALS treatment.

The paper investigates oligogenic risk in ALS using genome sequencing data, finding that multiple rare variants in known ALS genes increase disease risk but not clinical outcomes.

The paper identifies biallelic variants in ARHGAP19 as a cause of motor-predominant neuropathy with conduction slowing in multiple families.