Sulagna Dia Ghosh

The paper uses village editing to study how genetic backgrounds affect the impact of schizophrenia-associated mutations in human neurons.

The paper identifies cell type-specific molecular changes in ALS patients, showing enrichment of genetic risk factors in extratelencephalic neurons and altered responses in oligodendrocytes and microglia.

The paper identifies a neuron-astrocyte gene expression program, SNAP, that declines in aging and schizophrenia, linking it to cognitive function and genetic risk factors.

The paper shows that reduced Kv8.1 expression in ALS motor neurons with SOD1(A4V) and C9orf72 mutations increases vulnerability to cell death by affecting metabolism and transport pathways.

This study combines Ngn2 overexpression with small molecule patterning to efficiently generate lower induced Motor Neurons (liMoNes) from hPSCs, achieving high yields and functional characteristics.

This study identifies genetic regulators of DNA replication timing in human pluripotent stem cells, revealing a histone code and combinatorial regulatory mechanisms.

The paper identifies a common genetic variant in IFITM3 that explains most inter-individual variation in neural progenitor cell susceptibility to Zika virus using natural genetic variation and synthetic perturbations.

This study performs whole genome sequencing of human embryonic stem cells to identify genetic variants and provides resources for cell line selection.

Census-seq pools cells from >100 human donors into "cell villages" and quantifies donor DNA before and after selection to map genetic effects on cellular traits.

The paper presents twelve hiPSC lines with extreme polygenic risk scores for schizophrenia, available for CRISPR-based functional studies.

The paper identifies an enrichment of rare protein-truncating variants in ALS patients, highlighting novel genes like DNAJC7 and known ALS genes such as SOD1, NEK1, and FUS.

The paper identifies activity-based checkpoints that maintain olfactory circuit stability by regulating interneuron survival and dendrite branching during adult neurogenesis.