Trent M. Woodruff

This paper identifies naturally-encoded signaling bias at C5aR1 and C5aR2 receptors through structural and functional analyses, revealing molecular mechanisms underlying biased signaling in GPCRs.

This study shows that an AGE-rich diet during adolescence impairs memory via hippocampal synaptic deficits and microbiome changes, which can be mitigated by AGE inhibitors.

This study shows targeting C5aR1 reduces radiation-induced intestinal injury by promoting macrophage phenotypes that decrease stem cell apoptosis and improve tumor response.

This study shows that inhibiting C5aR1 reduces radiation-induced cognitive decline in mice, improving memory and reducing neuroinflammation without affecting tumor treatment.

This study shows paraquat enables α-synuclein to trigger NLRP3-dependent pyroptosis in microglia, linking environmental toxins to Parkinson's disease pathogenesis.

This study identifies Per1 as a systemic regulator of circadian stability, showing that its loss accelerates clock realignment and protects against jetlag-related disruptions.

This study identifies a convergent molecular mechanism and species-specific pharmacology in complement anaphylatoxin receptors through structural and functional analyses of ligand-receptor interactions.

The paper shows microbial amyloids from gut pathogens can trigger microglial hyperactivity and neuroinflammation, contributing to Alzheimer's disease progression.

This study examines the impact of a heterozygous Csf1r mutation on brain development and neuropathology in mice, showing reduced microglial abundance and altered gene expression in disease models.

This study identifies a neural circuit involving the pedunculopontine nucleus that modulates movement and gait in Parkinsonian mice, showing that targeting this circuit can alleviate motor symptoms.

This study shows senolytic drugs reduce brain aging and COVID-19-related neuropathology by targeting senescent cells in human brain organoids and mice.

This study shows SARS-CoV-2 activates microglial NLRP3 inflammasome via spike-ACE2 interaction, potentially linking viral infection to neurological symptoms like Parkinson's.

This study shows that removing RAGE signaling in SOD1G93A mice slows ALS progression, extends survival, and reduces neuroinflammation and oxidative stress.

The paper develops and validates a quantitative method using sodium fluorescein to assess BBB and BSCB integrity in neurodegenerative disease models, showing increased permeability in specific disease models.