Welcome to The Koliatsos Lab!

Our Research Interests

Founded in the late 1980s, our Lab explores the fundamental mechanisms of neural responses to traumatic and degenerative signals and works to identify targets for treating injury/degeneration with small molecules, peptides and cells. We currently focus on traumatic and degenerative axonopathies of the white matter as they occur in traumatic brain injury (diffuse axonal injury), major neurodegenerative diseases such as Alzheimer’s disease and conditions such as hypoxic ischemic encephalopathy and demyelination. We are especially interested in the role of the MAPK cascade of injury, NAD metabolism and SARM1 signaling and their convergence on Wallerian degeneration.

Our History

  • We are part of the legacy of Don Price and Mahlon DeLong featured by breakthrough discoveries in mechanisms of neurodegenerative diseases, primarily Alzheimer’s disease (AD), Parkinson’s Disease, and Amyotrophic Lateral Sclerosis (ALS)
  • In the 90s, we defined molecular mechanisms of neuronal survival and repair based on trophic peptide signals and signals related to apoptosis
  • In early 2000, we moved from trophic peptide signals to the role of stem cells in neural repair. We found evidence for a universal regenerative capacity 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 ALS and  
  • In 2010 we turned to complex models of neurotrauma. We developed a model of blast injury to brain and determined key factors in pathogenesis, including traumatic axonal injury and the role of vascular factors. We also developed a mouse model of mild TBI based on impact acceleration. We also and characterized unique features of diffuse axonal injury in the brains of veterans with blast histories
  • Our present emphasis is mechanisms of chronic traumatic axonopathies and their transsynaptic effects. We focus on interference with DLK and SARM-1 related cascades with gene editing and small-molecule therapeutics.
  • We view trauma not only as an important biological/clinical problem in and of itself, but also a model to better understand neurodegeneration in Alzheimer’s disease and related neurodegenerative dementias (ADRD). We are also developing models to explore the transition from TBI to ADRD

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 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, 1 R01 NS114397, and funds from Maryland Technology Development Corporation, American Health Assistance Foundation, Muscular Dystrophy Association, Congressionally Directed Medical Research, US Army MRDC, a Hopkins Discovery Award, the Kate Sidran Family Foundation and the Spyros N. Lemos Memorial Fund.