Tracy L. Young‐Pearse

This study develops a high-throughput platform using human cerebral organoids to screen for compounds that reverse HSV-1-induced neuroinflammation biomarkers associated with Alzheimer's disease.

This study shows that INPP5D/SHIP1 regulates endo-lysosomal function and cargo-selective phagocytosis in human microglia, linking its dysfunction to Alzheimer's disease pathology.

This study identifies BAG3's role in astrocytic proteostasis in Alzheimer's disease by showing its interactions with autophagy, proteasome, and retromer components, and its impact on Aβ clearance.

The paper introduces a proteomic tool to identify protein markers for human microglial states and validates their utility in purification and differentiation.

The paper identifies a novel astrocyte state linked to cognitive decline in Alzheimer's disease and validates its regulators through multi-modal analysis and mechanistic experiments.

The paper uses iPSC-derived astrocytes to study genetic risk factors for Alzheimer's disease, finding concordant molecular changes in both astrocytes and brain tissue.

This study shows ZCCHC17 regulates RNA splicing in neurons and its dysfunction contributes to splicing abnormalities in Alzheimer's disease, with potential therapeutic implications.

This study identifies GSDME as a mediator of mitochondrial damage and axon loss in neurodegenerative diseases, showing its role in ALS and FTD models.

This study shows that INPP5D/SHIP1 regulates inflammasome activation in human microglia, with reduced INPP5D leading to increased IL-1β and IL-18 secretion.

This study shows that SORL1 loss reduces APOE levels specifically in neurons and astrocytes, linking SORL1 and APOE to Alzheimer's disease risk through distinct pathways.

The paper identifies cell-type and cell-subtype specific eQTLs in aging human cortex, revealing variant effects on gene expression and disease associations.

The paper identifies small molecule inducers of miR-132 in human iPSC-derived neurons using HTS-HTS, showing neuroprotective effects against neurodegenerative phenotypes.

The paper identifies JMJD6 and other key drivers of Alzheimer's disease using predictive network analysis and validates their effects on amyloid-beta and tau pathology in human neurons.

The paper quantifies mosaic loss of chromosome Y (LOY) in brain cells across multiple datasets and finds microglia are most affected by LOY, with associated gene expression changes linked to aging and neurodegeneration.

This study identifies tau pathology-driven chromatin organization changes in aged human brains and shows these effects can be reversed with HSP90 inhibitors.

This study identifies splicing variations in aging brains linked to Alzheimer’s Disease, finds genetic regulation of splicing, and highlights shared pathways with other neurodegenerative diseases.

Molecular network analysis of RNA sequencing data from the aging human cortex identifies new Alzheimer's and cognitive decline genes.

The paper shows that Aβ oligomers from AD brain bind to synapses and disrupt synaptic activity, and this requires APP.