The Koliatsos Laboratory

Current Projects

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  • Animal models of diffuse axonal injury: traumatic axonopathy, neuroinflammation and proteinopathy
    • Models of simple and repetitive diffuse mild TBI (mTBI) in mice using a modified version of impact acceleration: diffuse TBI featured by traumatic axonal injury and neuroinflammation with a strong TBI dose-response profile; optic and corticospinal tracts as an especially vulnerable model systems for further studies into mechanisms and experimental therapeutics for traumatic axonal injury; the role of specific kinase pathways in mediating axonal and perikaryal degeneration in diffuse TBI


    • Retrograde degenaration of retinal ganglion cells associated with traumatic optic axonopathy after repetitive mild TBI (sham, A and increasing burden from B to D)

    • High-resolution neuroanatomical methods in characterizing neuropathology after diffuse mTBI: CLARITY in Thy1-eYFP-H mice, EM, expansion microscopy
    • Models of genetic vulnerability to chronic traumatic encephalopathy (CTE): exposure of two types of transgenic mice prone to tauopathy (P301S tau mice and 6-isoform wild-type human tau mice to repetitive mTBI); many-fold increase of tauopathy depending on mTBI burden


    • Tauopathy (green) and degeneration of retinal ganglion cells (red) worsen with repetitive mild TBI (from 1x to 12x)


  • Animal models of blast injury to brain (with APL)
    • Shockwave models of laboratory blast TBI, with emphasis on neuropathological and behavioral deficits: protection by shielding of torso with Plexiglas gear, but not head helmet; further exploration of protective body shielding that can be worn by exposed individuals; exploration of systemic (vascular, inflammatory) factors influencing outcomes in blast or non-blast polytrauma

    • Traumatic axonopathy with axon bulbs in the corticospinal tract after blast injury


  • Human neuropathology of blast, contusional and diffuse axonal injury
      Typical diffuse axonal injury after motor vehicle crash (top) and blast (middle) compared to few linear swellings in opiate overdose (bottom)
    • Veterans with blast histories: diffuse axonal injury with unusual, honeycomb-patterned, perivascular APP (+) abnormalities in medial dorsal frontal white matter and elsewhere; association of such abnormalities with reactive microglia; a new type of diffuse axonal injury?
    • Neuropathological and finite element modeling (with the Whiting School of Engineering) of blast TBI: compressive forces in the thoracic and abdominal cavities that rapidly increase pressure in the superior vena cava-jugular system
    • Neuropathology of the cortical and subcortical frontal connectome in contusions and diffuse axonal injury: time course of retrograde and transsynaptic changes of injury and degeneration
    • Hopkins News Media Release, 2014
      Combat Veterans' Brains Reveal Hidden Damage from IED Blasts
    • USA Today, 2015
      Bomb-induced brain injury may be its own disease
    • Washington Post, 2015
      Wounds of war that never heal
    • Reuters.com video - August 13, 2015
      Hidden Damage Revealed in Veterans' Brains


  • Protection of diffuse axonal injury with kinase inhibitors (with Wilmer Eye)
    • DLK-JNK signaling cascade as mediator of acute and chronic effects of traumatic axonal injury, i.e. axonal and neuronal degeneration, disconnection, neuroinflammation and proteinopathy: genetic and pharmacological studies

    • Retinal ganglion cells labeled with gamma synuclein (top) and corticospinal pyramids retrogradely labeled with cholera toxin B (bottom) (both red) express activated p-c-jun (green) in the nucleus after diffuse mTBI.

  • Tau proteomics
    • Changes in post-translational modifications and interactions in protein networks in response to TBI: characterization of tau fragments in CSF and brain tissue with immunoprecipitation, gel electrophoresis, phosphoprotein columns, and MALDI or SELDI-TOF techniques

  • Stem cell therapies for traumatic axonal injury

      Human embryonic stem cell-derived neurons expressing the Channel rhodopsin gene (green) to allow optogenetic functional analysis. Panels show individual (top) and clustered (bottom) neurons 57 days after transfection of their precursor cells.

    • Regenerative therapies based on human oligodendrocyte progenitor cell (hOPC) transplants: massive migration into white matter tracts and ensheathment of host axons that is very different from fates on transplanted human neuronal progenitors (hNPs)
    • Regenerative therapies based on combined transplants of hOPCs and hNPs in CNS motor circuits using optogenetic strategies to ascertain the functionality of new circuits