Li Gan

This study shows that TDP-43 mutations in ALS/FTD reduce HSV-1 infection by disrupting cell-adhesion pathways and impairing viral entry.

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

This study shows that transplanting wild-type human iPSC-derived microglia into progranulin-deficient mice reduces neuropathology, circuit dysfunction, and behavioral issues in a FTD model.

This study identifies cGAS as a key mediator of TDP-43 pathology in ALS and shows that its inhibition reduces RNA splicing defects and neurodegeneration.

This study identifies soluble DLK1 from senescent microglia as a factor impairing oligodendrocyte function and altering neuronal activity in aging.

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.

The paper develops a high-resolution spatial long-read sequencing method and software to analyze isoform variability in brain cell types, revealing both region-specific and cell-type-specific patterns.

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 introduces ScISOr-ATAC to measure splicing and chromatin accessibility in frozen brain tissues, finding convergent and divergent patterns in different cell types and conditions.

This study shows that CT-KIBRA repairs synaptic plasticity and memory in tauopathy models by stabilizing PKMζ, without altering tau levels or preventing synapse loss.

The paper develops a high-throughput single-cell genomics approach to study age-related and Alzheimer's disease-associated cell population dynamics and molecular signatures in human and mouse brains.

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 caspase inhibition reduces tau cleavage and neurotoxicity in iPSC-derived neurons with the V337M MAPT mutation.

This study uses a CRISPRi/a platform in iPSC-derived microglia to identify genes regulating microglia states and their therapeutic targets.

The paper identifies a Csf1r-independent microglial subset in adult mice that exhibits progenitor-like features and is distinct from homeostatic microglia.

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 identifies p300/CBP as a regulator of tau secretion via the autophagy-lysosomal pathway, showing its role in tau propagation in tauopathies.

Long-read sequencing with the knock-knock pipeline profiles CRISPR knock-in repair, finding perfect homology-directed repair is often a minority of integration events and mis-integration varies by context.

The paper identifies cis-regulatory chromatin contacts in neural cells and links them to genetic variants associated with complex neurological disorders.

This study shows that adult microglia self-renew to restore homeostasis after ablation, with specific maturation programs and spatial organization.