Jason C. Dugas

This study shows lysosomal health influences myeloid cell states and immune responses, with Grn deficiency leading to lysosomal dysfunction and specific transcriptional changes in microglia.

This study shows chronic NLRP3 inflammasome activation leads to neutrophil entry into the brain and interactions with microglia, contributing to CNS pathology.

This paper demonstrates that dual targeting of TfR and CD98hc enhances brain exposure of large molecules compared to single-target approaches.

This study shows that GPR34 regulates microglia function and loss-of-function in TREM2 KO microglia rescues cholesterol metabolism, suggesting GPR34 as a therapeutic target for Alzheimer's disease.

This study investigates TfR-mediated BBB transport in mice across development and aging, finding elevated transport in early development and stability across adulthood, including in an AD model.

This study develops an antibody transport vehicle targeting the transferrin receptor to improve brain delivery of anti-amyloid antibodies, reducing ARIA-like lesions and vascular inflammation in a mouse model.

This study compares the biodistribution of Fc-engineered molecules targeting BBB receptors with standard antibodies, showing distinct CNS and peripheral organ targeting.

This study shows SARM1 causes calpain-dependent dendrite degeneration in mouse hippocampal neurons, revealing distinct degeneration pathways in axons and dendrites.

This paper demonstrates that systemically delivered OTV, a TfR-binding molecule, effectively transports ASO across the BBB, achieving widespread and sustained knockdown of target genes in the CNS of mice and non-human primates.

The paper compares brain delivery and efficacy of two TfR-targeted enzyme fusions in MPS II mice, finding the moderate-affinity ETV:IDS has better brain exposure and substrate reduction than the high-affinity IgG:IDS.

This paper characterizes microglial metabolic changes in an APP knock-in mouse model of AD, finding lipid dysregulation and immunometabolic perturbations linked to fibrillar Aβ.