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

Spatial dynamics of spinal cord injury-elicited glial cell activation. For more, please see our  2018 review in  Neurotherapeutics  .

Spatial dynamics of spinal cord injury-elicited glial cell activation. For more, please see our 2018 review in Neurotherapeutics.

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.

 
We revealed recently that spinal cord injury disrupts the circadian system. Please see our studies published in   eNeuro   and in   J. Neurotrauma  .

We revealed recently that spinal cord injury disrupts the circadian system. Please see our studies published in eNeuro and in J. Neurotrauma.

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.

 
Successful axon regeneration requires growth-promoting responses by the injured neuron and by its local environment. Please see our   J. Neuroinflammation  review on axon degeneration and regeneration.

Successful axon regeneration requires growth-promoting responses by the injured neuron and by its local environment. Please see our J. Neuroinflammation review on axon degeneration and regeneration.

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.


One ongoing project involves the microRNA miR-155. We found that miR-155 deletion was protective after SCI: miR-155 deletion improved both neuroprotection and axon plasticity, and led to improved locomotor recovery. We are currently assessing the reparative potential of a clinically feasible miR-155 inhibitor.

In addition to studying SCI, we have also performed behavioral neuroscience research related to mood and metabolic disorders. Our lab plans to develop models and collaborations to study these and other conditions further.