The Gaudet lab aims to reveal links between molecular, cellular, and behavioral changes elicited during neuropathology. We have several research interests:

1. Neuroinflammation. Spinal cord injury (SCI) causes massive neuroinflammation, which can worsen pathology ("secondary damage"). We seek to better understand the post-SCI cascades that drive inflammation, and to shift the inflammatory response to better preserve/repair tissue and improve behavioral outcomes.

2. Biological clocks. Our work has shown that SCI can broadly disrupt function across peripheral organs. SCI disrupts molecular rhythms (e.g., in spinal cord, liver, and blood) that occur in parallel with altered diurnal rhythms in behavior. Ongoing work seeks to understand related mechanisms and potential treatments that boost rhythm recovery.

3. Axon plasticity and regeneration. After SCI, central nervous system axons fail to regenerate. This is due to a poor neuron-intrinsic growth response, and ineffective neuroinflammatory and glial dynamics. Improving post-SCI plasticity of these axons could enhance recovery of function.

Fonken LK, Frank MG, Gaudet AD, Maier SF. Stress and aging act through common mechanisms to elicit neuroinflammatory priming. Brain, Behavior, and Immunity. 2018;pii:S0889-1591(18)30334-9.

Gaudet AD, Fonken LK. Glial cells shape pathology and repair after spinal cord injury. Neurotherapeutics. 2018.

Fonken LK, Frank MG, Gaudet AD, D’Angelo HM, Daut RA, Hampson EC, Ayala MT, Watkins LR, Maier SF. Neuroinflammatory priming to stress is differentially regulated in male and female rats. Brain, Behavior, and Immunity. 2018;pii:S0889-1591(18)30049-7. 

Bateman EM, Schleicher WE, Smith EJ, Sweet DR, Gaudet AD. Journal Club: MRI reveals acute inflammation in cortical lesions during early MS. Neurology. 2018;90:e724-726.