Indigo V.L. Rose

The paper identifies ANO3-ITPR1 signaling as a caspase-independent mechanism for synaptic phosphatidylserine exposure, which controls synapse pruning during development and neurodegeneration.

The paper shows ECM proteolysis, specifically via MMP14 and brevican, maintains dynamic synapse plasticity during brain development in zebrafish and human iPSC-derived cultures.

The paper introduces the Neurolipid Atlas, a lipidomics resource for neurodegenerative diseases, revealing that ApoE4 impairs astrocyte reactivity by promoting cholesterol ester accumulation.

This study shows that β-amyloid induces microglial GPC4 and APOE, which increases neuronal tau pathology and toxicity.

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 EV miRNAs from WT mice improve sociability in immunodeficient mice by modulating synaptic function and immune-neuron communication.

The paper introduces CrAAVe-seq, an AAV-based CRISPR screening platform for in vivo cell type-specific analysis, demonstrating its scalability and sensitivity in identifying neuron-essential genes.

The paper identifies and characterizes a reference iPSC line, KOLF2.1J, for standardized use in collaborative studies across multiple differentiation protocols and assays.

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

This study develops a fluorescent Aβ analogue to monitor glial cell phagocytosis of amyloid β in real time, showing microglia uptake exceeds astrocytes.