Patrick G. Sullivan

The paper investigates delayed glucose metabolism changes in APP/PS1 KI mice after closed-head injury, finding increased pyruvate and lactate labeling in cortex and hippocampus 8 months post-injury.

The paper identifies ceramide-rich extracellular vesicles as biomarkers of traumatic brain injury, showing their role in inflammation and neuronal mitochondrial dysfunction.

This study examines sex-specific mitochondrial changes in a mouse model of traumatic brain injury, revealing distinct spatial and temporal responses in mitochondrial function across brain regions.

This study shows astrocytes transfer mitochondria to neurons after TBI to support mitochondrial function in neuronal soma, dendrites, and axons but not synapses, and demonstrates therapeutic potential of exogenous mitochondrial transfer via extracellular vesicles.

This study shows that traumatic brain injury worsens mitochondrial dysfunction in APP/PS1 mice through time-dependent mechanisms, with sex differences in vulnerability.

This study compares fibroblast metabolism across species, finding spiny mice and rabbits exhibit a glycolytic preference and oxidative stress resilience across lifespan.

This study investigates how tau pathology affects metabolism and excitatory activity in mouse models, finding that it preserves glucose tolerance and shifts metabolic flux toward glutamate synthesis.