Mark Koontz

The paper develops human tri-lineage brain microtissues composed of neurons, astrocytes, and microglia, showing they recapitulate cell-cell interactions and pathological processes.

This study shows NLK disrupts nuclear import, causing TDP43 mislocalization in ALS, and suggests NLK as a therapeutic target.

The paper develops iAssembloids to study neuron-glia interactions using CRISPRi screens and finds GSK3β inhibits NRF2-mediated oxidative stress response and APOE-4 promotes neuronal activity.

The paper shows that loss of GRN in human brain organoids leads to TDP-43 pathology, driven by astrocytes, and can be rescued by progranulin.

The paper uses CRISPRi screens and single-cell transcriptomics in human astrocytes to identify regulators of inflammatory reactive states and their relevance in disease.