Click each project to view / hide details:
- NMNAT2-SARM1 signaling in traumatic axonopathy in the corticospinal and visual pathway; NMNAT2-SARM1 neurochemistry; genetic and pharmacological interventions for prevention and treatment of pathology and symptoms
- DLK-JNK signaling cascade as mediator of acute and chronic effects of traumatic axonal injury in perikarya and axons of the visual and corticospinal pathway; genetic and pharmacological interventions
![](http://labs.pathology.jhu.edu/wp-content/uploads/sites/19/2021/01/variety-of-pathological-configurations.jpg)
Acceleration injury in the optic tract generates a variety of pathological configurations including end-bulbs, spindle-like axonal swellings and more classical Wallerian-type fragmentation. It is unclear if the above are part of the same continuum or separate biological entities.
![](http://labs.pathology.jhu.edu/wp-content/uploads/sites/19/2021/01/wallerian-dgeneration-optic-nerve.jpg)
Wallerian degeneration in the optic nerve after acceleration TBI (top). Knocking out DLK and LZK protects the proximal axonal segments of injured axons (bottom)
![](http://labs.pathology.jhu.edu/wp-content/uploads/sites/19/2019/04/axonopathies3.png)
Induction of the dual lineage kinase DLK (top) and downstream phosphorylation of c-JUN (bottom) in injured optic nerve and retina
![](http://labs.pathology.jhu.edu/wp-content/uploads/sites/19/2021/01/airyscan-corticospinal-axons.jpg)
High-resolution Airyscan rendition of corticospinal axons (bottom left) from the YFP-H mouse that shows an excellent visualization of the corticospinal tract (top right)
- Effects of NAMPT inhibitors to prevent Wallerian degeneration–mechanisms
- Effects of DLK inhibitors to prevent Wallerian degeneration—mechanisms
- Effects of other interventions, i.e. NMPT inhibitors plus NaR
![](http://labs.pathology.jhu.edu/wp-content/uploads/sites/19/2021/01/nmpt-inhibitors.jpg)
Different classes of NMPT inhibitors protect axotomized axons from Wallerian degeneration. DMSO is vehicle.
- Neuropathological characterization of behind-helmet blunt TBI in pigs, with emphasis on meningeal and parenchymal macro- and micro-hemorrhages and diffuse axonal injury; correlations among impact severity, meningeal and parenchymal pathology and clinical outcomes
![](http://labs.pathology.jhu.edu/wp-content/uploads/sites/19/2019/04/helmet.jpg)
Diffuse axonal injury in the medullary tegmentum in a pig that became critical after ballistic trauma to the head (APP)
![](http://labs.pathology.jhu.edu/wp-content/uploads/sites/19/2021/01/distribution-map-brain-stem-lesions.jpg)
distribution map of brain stem lesions in another case
- Exploration of Frequency Following Response as a specific neurophysiological/audiological marker of concussion; predictive modeling using machine learning classifiers; correlations with neuropathology and clinical outcomes
![](http://labs.pathology.jhu.edu/wp-content/uploads/sites/19/2019/04/biomarkers.jpg)
Differences in auditory brain response between normal (light blue) and TBI subjects (purple) based on frequency domain transform (with Amanda Lauer and Clara Scholl)
- Generation of second-generation models of concussion (founded on the classical Marmarou paradigm) that allow concomitant dialing of impact and acceleration and related measurements with minimal experimenter involvement
- Neuropathology of the cortical frontal and subcortical connectome in contusions and diffuse axonal injury: retrograde and transsynaptic neuronal changes signifying injury and degeneration
![](http://labs.pathology.jhu.edu/wp-content/uploads/sites/19/2019/04/proj6.jpg)
Thalamic degeneration (SMI310 staining) after contusions in orbitofrontal and temporopolar cortex indicated on the right