Photo of Stephen J. Crocker, Ph.D.

Stephen J. Crocker, Ph.D.

Associate Professor, Neuroscience
Director, Neuroscience Graduate Program
Academic Office Location:
UConn Health
263 Farmington Avenue
Farmington, CT 06030
Phone: 860-679-8750

Crocker Lab

Neuroscience Graduate Program

B.Sc.University of King's CollegeBiology
Ph.D.University of OttawaPharmacology
PostdocOttawa Hospital Research InstituteNeurodegeneration
PostdocThe Scripps Research InstituteNeuropharmacology
PostdocThe Scripps Research InstituteImmunology

Post-Graduate Training
FellowshipOntario Neurotrauma FoundationPostdoctoral Fellowship
FellowshipNational Multiple Sclerosis Advanced Postdoctoral Fellowship
PostdoctoralNeuroscience Research InstituteNeuroscience
PostdoctoralThe Scripps Research Institute Neuropharmacology
PostdoctoralThe Scripps Research InstituteImmunology

Name of Award/HonorAwarding Organization
Osborn Award for Excellence in Graduate Teaching in Biomedical ScienceThe Graduate School, UConn Health
National Multiple Sclerosis Society Career Transition Award (2007-2011)National Multiple Sclerosis Society
Dale McFarlin Travel Award National Multiple Sclerosis Society
International Outstanding Young Investigator Award ICCP
Bronze MedalOttawa Life Sciences Conference
Jock Cleghorn Award. Canadian College of Neuropsychopharmacology (CCNP)
Summer Studentship Parkinson’s Disease Foundation
Name & DescriptionCategoryRoleTypeScopeStart YearEnd Year
National Multiple Sclerosis Society Biomedical Research Committee AStudy SectionStanding MemberExternalInternational20172020
American Association of Neuropathologists Professional/Scientific OrganizationMemberExternalNational2005
American Society of Neurochemistry Professional/Scientific OrganizationMemberExternalNational2003
Society for Neuroscience Professional/Scientific OrganizationMemberExternalNational1999

Stem cells; glia; metalloproteinases; cytokines; development; pathology; tissue culture.

My lab is interested in how the immune and nervous systems interact and how this balance is disrupted in diseases of the nervous system. The ultimate aim of our research program is to understand how the brain is injured during chronic inflammatory diseases of the nervous system, what regulates the ability of the brain to repair itself and how this knowledge might be used to promote brain regeneration and recovery.

Our current projects are examining role of the immune system in myelin pathology as it relates to diseases like Multiple Sclerosis (MS). In MS, the immune system mounts an inappropriate response against the coating of the nerve cells, called myelin. Myelin is critical for proper brain development and function. Hence, progressive myelin injury in MS can result in debilitation that can lead to permanent disability. The cause of MS is not known.

The purpose of this research is to understand how the nervous system responds to myelin injury and repairs myelin damage. Toward this goal, we have found that during an inflammatory attack that causes myelin damage the nervous system produces a protein called Tissue Inhibitor of Metalloproteinases-1 (TIMP-1). A function of TIMP-1 is to block key enzymes, called metalloproteinases, immune cells use to move into the brain tissues and can breakdown myelin. Our studies indicate that during inflammatory models of myelin injury TIMP-1 may be important in the regulation of immune cells called macrophages and microglia. As well, we determined that following myelin injury mice that lack TIMP-1 are also less able to repair their myelin. Accordingly, we propose to study two primary functions we believe to be important roles for TIMP-1: the control of macrophages and microglia following myelin injury, and the stimulation of myelin repair through promoting endogenous cells to rebuild the injured myelin.

It is interesting to note that although basal expression of TIMP-1 in the adult CNS is very low, it is readily and consistently induced in a variety of rodent demyelination models and increased in human individuals with acute demyelinating encephalomyelitis. However, levels of TIMP-1 are not elevated in chronic progressive forms of MS. It is plausible that chronic CNS inflammation, as occurs in MS, attenuates the ability of the brain to express TIMP-1 and the down-regulation of TIMP-1 may contribute to an individual’s susceptibility to developing CNS demyelination. Indeed, a paucity of TIMP-1 has also been reported with a chronic virus infection of the brain. Accordingly, we propose that study of TIMP-1 may represent an important system to understand MS-related CNS pathology.

Accepting Lab Rotation Students: Summer 2022, Fall 2022, and Spring 2023

Lab Rotation Projects
Research rotation projects in the lab will address the following questions:
Project 1. Does TIMP-1 participate in the regulation of CNS myelination?
Project 2. How does TIMP-1 regulate microglial responses to injury? Project 3. What controls astrocytic TIMP-1 expression?

Journal Articles