Mathew M. Blurton-Jones

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.

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

The paper examines proteasome composition and activity in human iPSC-derived cortical neurons from early-stage sporadic Alzheimer's disease patients, finding increased 20S proteasome assemblies and proteolytic activity.

This study shows DNA damage in neurons leads to a senescent-like state similar to Alzheimer's disease, with distinct features from fibroblasts.

The paper investigates the role of LACTB in Alzheimer's disease risk through Mendelian Randomization and experimental models, finding reduced LACTB expression lowers AD risk and increases succinylcarnitine levels.

This study shows PPARδ activation in microglia reduces inflammation and enhances phagocytic function, shifting microglia toward a disease-associated state in neurodegenerative models.

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 microglia-dependent and independent mechanisms of lipid dysregulation in Alzheimer's disease using mouse models and lipidomics.

The paper identifies a microglia population that takes up circulatory proteins, enhancing phagocytosis and innate immunity through ApoA-I uptake.

The paper investigates the role of microglia in maintaining blood-brain barrier properties in health and finds that microglia are not required, but PLX5622 treatment affects endothelial cholesterol metabolism.

The paper introduces an organelle phenotyping approach using live-cell microscopy to identify C1q as a regulator of microglial function, showing its role in fatty acid storage and mitochondrial membrane potential.

This study shows that ER and SOCE Ca2+ signals are not required for directed migration of human microglia in response to purinergic stimuli, suggesting a Ca2+-independent mechanism involving cyclic AMP.

This study investigates mitochondrial dysregulation's role in neurodegeneration after contusion injury using a 3D in vitro triculture model of human brain cells.

This paper develops a platform to model and manipulate human microglial states in vitro using single-cell RNA sequencing and genetic tools, identifying disease-associated transcriptional signatures.

This study compares HD astrocytes from human iPSCs and mouse models, identifying dysregulated synaptogenesis, actin signaling, and maturation, with unique human findings and potential therapeutic targets.

This study shows that TREM2 loss in human iPSC-derived microglia leads to altered Ca2+ signaling and motility via purinergic receptor pathways.

This study investigates a kinase-dead Csf1r mutation in mice, showing it causes dominant-negative effects on CSF1R signaling and impacts macrophage development and brain microglia.

This study investigates the ability of the quorum sensing peptide PapRIV to activate BV-2 microglia and cross biological barriers, showing in vitro activation and in vivo presence.

This study examines C9orf72 ALS/FTD patient-derived iPSC-microglia mono-cultures, finding they form RNA foci, have reduced C9orf72 protein, and show endosomal-lysosomal dysfunction, but no significant microglial-enriched gene expression differences.