Wenjie Luo

This study identifies TRAPPC8 as a brake on UFMylation that suppresses tauopathy by interacting with UBA5, showing its therapeutic potential in Alzheimer's disease.

The paper develops a humanized neuroimmune model to study tauopathy and identifies microglial and lncRNA mechanisms that protect neurons.

The paper develops a neuron-specific interactome map in human excitatory neurons to identify novel risk genes and pathways in Alzheimer's disease.

This study identifies cGAS-mediated IFN-I signaling as a driver of disease progression in drug-refractory epilepsy, showing that targeting cGAS reduces epileptic phenotypes and inflammation.

The paper identifies a STING-IFN-CH25H lipid axis linking innate immune activation to tau pathology and shows its role in neurodegeneration.

This study shows that DAP12 deficiency reduces tau-induced inflammation and myelin loss in mice, despite increased tau pathology, by altering microglia-oligodendrocyte interactions.

This study identifies mitochondrial complex III-derived ROS as a key driver of immunometabolic changes in astrocytes that contribute to dementia pathology.

This study combines APOE4 and TREM2R47H in female tauopathy mice to identify pathways activated by AD risk factors, finding cGAS-STING signaling and microglial senescence as potential drivers.

The R136S mutation on APOE3 enhances resistance to tau-related pathology and toxicity by downregulating the cGAS-STING-IFN signaling pathway.

The paper creates a human iPSC model of 4R tauopathy and identifies genetic modifiers of Tau propagation using CRISPRi screening.

The paper identifies sex-biased transcriptomic responses in aged demyelination, showing Tlr7 mediates these differences through interactions with sex chromosomes and gonads.

This study shows that microglial NF-κB signaling drives tau spreading and toxicity in a mouse model of tauopathy, with inhibition reducing tau pathology and cognitive deficits.

The paper maps Tau interactomes in neurons using APEX and AP-MS to reveal activity-dependent interactions and FTD mutation effects on mitochondrial associations in neurodegenerative diseases.

The paper introduces SnISOr-Seq, a method for single-nuclei isoform RNA sequencing, and finds distinct combination patterns of transcript elements in human brain cell types.

This study shows that PGRN deficiency affects amyloid-beta levels and microglial activation in a sex- and age-dependent manner, influencing lysosomal activity and inflammation in Alzheimer's disease.

This study identifies GSAP's role in Alzheimer's disease by showing it regulates mitochondrial function through the MAM and lipid homeostasis, with a SNP linked to increased AD risk.

The paper identifies brain-region specific splicing patterns at single-cell and spatial resolution in postnatal mice, revealing cell-type specific and region-specific isoform expression.

This study identifies R47H-TREM2 mutation-induced proinflammatory microglial states in human AD and tauopathy mice, showing Akt pathway involvement and potential therapeutic targets.

This study shows that 25-HC enhances IL-1β production in microglia, particularly in apoE4-expressing cells, suggesting a role in AD neuroinflammation.

The paper introduces ScISOr-Seq, a method combining single-cell full-length cDNA amplification with short-read and long-read sequencing to identify isoforms in cerebellar cell types across thousands of cells.