Su‐Chun Zhang

The paper fine-maps PD GWAS signals across cell types, revealing convergent glial-neuronal risk genes and a shared vesiculopathy network.

This study uses single-nucleus multiomic sequencing to analyze gene expression and chromatin accessibility in the Down syndrome prefrontal cortex, revealing widespread dysregulation in metabolic, synaptic, and neuroinflammatory pathways.

This study identifies GFAP as a novel mediator of mitochondrial fission by surrounding fission sites and modulating Drp1 recruitment, revealing a new mechanism in mitochondrial plasticity.

This study shows transplanted human cortical neurons can integrate into and repair damaged motor circuits in ischemic mice by following transcriptional codes for axon guidance and synapse formation.

The paper uses single-nucleus sequencing to identify oxidative stress and metabolic changes in Down syndrome basal forebrain neurons at birth.

This study shows that loss of IVNS1ABP causes a progeroid neuropathy by impairing proteostasis, leading to protein aggregation and lysosomal dysfunction in neuronal cells.

This study identifies reduced WNT signaling in Down syndrome progenitors, leading to fewer COUP-TFII+ interneurons and impaired neurogenesis.

The paper develops a chemical cocktail to induce senescence in iPSC-derived neurons to better model age-related neurodegenerative disorders.