Welcome to The Koliatsos Laboratory!

Research Interests

Founded in the late 1980s, our Lab has been exploring the fundamental mechanisms of neural responses to traumatic and degenerative signals as well as mechanisms of neural repair. Our current interests include: traumatic brain injury and models; mechanisms and treatments of traumatic axonopathies; molecular neuropathology of traumatic brain injury; and regeneration of circuits in the injured brain using stem cells and their products.

Our History

Terminal boutons containing synaptophysin (black) from a differentiated human neural stem cell graft synapse with the cell body of a rat motor neuron

  • In the 90’s, we led efforts in defining molecular mechanisms of neuronal survival and repair based on trophic peptide signals and signals related to programmed cell death (apoptosis)
  • We were part of the legacy of Don Price that made breakthrough discoveries in mechanisms of neurodegenerative diseases, primarily Alzheimer’s disease (AD) and Amyotrophic Lateral Sclerosis (ALS)
  • In the early 2000s, we explored the role of stem cells in neural repair, focusing on stem cell transplants as well as endogenous niches. We found a more or less universal regenerative responsiveness of the nervous system, including regions previously thought to lack growth signals. Some of this work prompted the first clinical trial of stem cell therapy in a major neurodegenerative disease (ALS).
  • We have recently turned to complex models of neurotrauma. With colleagues at the Applied Physics Laboratory (APL), we developed a mouse model of blast injury to brain and determined key factors in pathogenesis, including traumatic axonal injury and the role of systemic factors.
  • We also developed and characterized a mouse model of mild TBI based on impact acceleration and characterized some unique features of diffuse axonal injury in the brains of veterans with blast histories. Click here to read more.
  • Our present emphasis is mechanisms of chronic TBI such as traumatic axonopathy and its transsynaptic effects, neuroinflammation, and proteinopathy (tauopathy, amyloidosis). We also explore small-molecule and stem-cell therapeutics for diffuse axonal injury. We also continue our work in understanding and modeling blast TBI and developing protective strategies.

Axons of human neurons undergoing Wallerian degeneration on a microfluidic device after axonal injury. Neurons were differentiated from human embryonic stem cells.

Time lapse of fluorescent axons proximal to laser axotomy showing regenerative and degenerative responses over 16 hours.

Time lapse of fluorescent axons distally to laser axotomy showing Wallerian degeneration over 16 hours.

Our Funding
Work mentioned here has been funded by federal, state and other sources, primarily via NIA 2 P50 AG 05146, NIA 1 R35 AG 07914, NIA 1 P01 AG 10480, NINDS 5 P50 NS 20471, NINDS 2 R01 NS 10580, NIA 2 P50 AG 051461, RO1 NS 37145, NIA 3 P50 AG 05146, 1 RO1 AG 16263, R21MH064757, 1 R01 NS045140, R21MH3083792, 1 R01 EY028039, and funds from Maryland Technology Development Corporation, American Health Assistance Foundation, Muscular Dystrophy Association, Congressionally Directed Medical Research, a Hopkins Discovery Award, the Kate Sidran Family Foundation and the Spyros N. Lemos Memorial Fund.