Marina Hogan

This study shows that somatic DNA-repeat expansions in cortical and striatal neurons of Huntington's disease initiate similar pathological changes, but lead to distinct gene expression outcomes.

The paper analyzes single-nucleus RNA-seq data from the human striatum and prefrontal cortex to study inter-individual variation in cell abundances and gene expression, finding age-related changes and genetic associations.

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

The paper identifies genetic variants that influence neuronal responses to interferons by analyzing gene expression and STAT1 binding in iPSC-derived neurons.

The paper shows that HTT CAG repeats expand in striatal neurons over time, leading to gene expression changes and neurodegeneration in Huntington disease.

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.