Masashi Fujita

This study identifies 36 genetic loci associated with recurrent UTIs and highlights PSCA as a key gene involved in urinary epithelial defense against bacteria.

The paper identifies regulators of microglial activation states using CRISPR screens and single-cell transcriptomics, revealing functional roles of ZNF532, PRDM1, and DNMT1 in disease-associated microglial states.

The paper identifies two genes, ADRA1B and LY6E-DT, downregulated in excitatory neurons associated with neuroticism and found to partially mediate the risk of Alzheimer's disease.

This study evaluates six potential serum biomarkers for multiple sclerosis in at-risk individuals and finds most are not robust predictors, though SPP1 shows a significant inverse correlation with genetic risk.

The paper identifies cell type-specific gene modules associated with Alzheimer's Disease traits using snRNASeq data from human brain tissues.

The paper uses automated image segmentation to identify CD74high microglia associated with cognitive decline in AD, linking transcriptomic and morphological features.

The paper identifies microglia subsets in ALS brain and spinal cord, finding an undifferentiated phenotype and enrichment of interferon response microglia in aggressive cases.

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

The paper uses single-cell data to identify factors regulating an Alzheimer's disease-related microglial signature and proposes a new analytic framework for microglial classification.

The paper creates a brain-wide map of mitochondrial phenotypes by combining physical voxelization with biochemical profiling, revealing regional differences in mitochondrial density and function.

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 identifies 236 MS susceptibility variants and highlights neuronal and glial dysfunction as key factors in MS susceptibility.

The paper identifies AD-associated lncRNAs with spatial and cell-type-specific expression patterns and shows OIP5-AS1 contributes to microglial activation in AD.

The paper examines immunosenescence trajectories in diverse populations, finding associations between immunological age and brain atrophy, while highlighting CMV status and genetic ancestry as key factors.

The paper identifies Topoisomerase I inhibitors as immunomodulators for Alzheimer's disease by characterizing their effects on human microglial subtypes in vitro and in a zebrafish model.

The paper identifies disease-specific cell signatures in non-lesional brain tissue of MS patients using single-cell and spatial transcriptomics.

The paper identifies two distinct aging trajectories in the human brain linked to Alzheimer's disease or alternative aging, using single-nucleus RNA-seq data and causal modeling.

COOBoostR uses extreme gradient boosting to predict tumor tissue or cell-of-origin using chromatin marks and mutation density data, outperforming random forest methods in speed and accuracy.

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

This study identifies disease-enriched microglial subsets and validates compounds that modulate their states using single-cell RNA sequencing and in vitro experiments.

The paper analyzes HHV-6 integration in human genomes, identifies co-evolution with chr22q, and reports evidence of in vivo excision and reactivation.

The paper screens 12,503 Japanese CRC patients and 23,705 controls for germline variants in 27 cancer genes, finding 3.3% of patients have pathogenic variants linked to CRC risk.

The paper identifies hundreds of genes deregulated by SVs in cancer, showing increased expression linked to SV breakpoints and enhancer elements.

The paper uses whole-genome sequencing to predict cell-of-origin for primary liver cancers, finding heterogeneity in origin predictions across cancer types.

The paper analyzes immuno-genomic data across 31 cancer types to identify immune escape mechanisms and immuno-editing histories.