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Stephen Crocker, Ph.D. - University of Connecticut. Farmington, CT, US

Stephen Crocker, Ph.D.

Associate Professor of Neuroscience and Associate Director of Neuroscience Graduate Program | University of Connecticut


Prof. Stephen Crocker is an expert on how the immune and nervous systems interact and how this balance is disrupted.


Prof. Stephen Crocker is an Associate Professor of Neuroscience and the Associate Director of the Neuroscience Graduate Program. His 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 his 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.

His current projects examine the 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.

Areas of Expertise (3)

Nervous System

Immune System


Education (2)

University of Ottawa: Ph.D.

University of King's College: B.Sc.

Affiliations (3)

  • American Association of Neuropathologists
  • American Society of Neurochemistry
  • Society for Neuroscience

Accomplishments (2)

National Multiple Sclerosis Society Career Transition Award (professional)

National Multiple Sclerosis Society Career Transition Award (2007-2011) - National Multiple Sclerosis Society

Dale McFarlin Travel Award (professional)

Dale McFarlin Travel Award - National Multiple Sclerosis Society





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Dr. Deckers Award Nomination 2018: Stephen Crocker for Jody Gridley


Media Appearances (3)

Neural Stem Cells in MS Patients Look Prematurely Old

MedPage Today  online


Senescence was found in neural progenitor cells within demyelinated white matter lesions in progressive MS autopsy tissue, according to Stephen Crocker, PhD, of the University of Connecticut School of Medicine in Farmington, and colleagues...

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Brain stem cells age faster in multiple sclerosis patients: study

Xinhua  online


Stephen Crocker, a health neuroscientist at the University of Connecticut, and his colleagues found that brain stem cells from primary progressive MS patients look decades older than otherwise similar cells from healthy people of the same age...

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NYSCF Collaboration Uncovers New Target for Progressive Multiple Sclerosis Therapies

The New York Stem Cell Foundation  online


In this study, researchers discovered using PPMS patient stem cells that a phenomenon called “cell senescence” (which is most often associated with cellular aging) could play a role in PPMS by inhibiting the maturation of the cells that produce myelin. The team also identified a drug, rapamycin, that reverses cell senescence in stem cell models of the disease. The research, published in Proceedings of the National Academy of Sciences, was conducted by scientists at the University of Connecticut led by Stephen Crocker, PhD, in collaboration with the University of Edinburgh’s Anna Williams, PhD, and NYSCF Senior Research Investigator Valentina Fossati, PhD...

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Articles (5)

Extracellular vesicle fibrinogen induces encephalitogenic CD8+ T cells in a mouse model of multiple sclerosis

Proceedings of the National Academy of Sciences

2019 Extracellular vesicles (EVs) are emerging as potent mediators of intercellular communication with roles in inflammation and disease. In this study, we examined the role of EVs from blood plasma (pEVs) in an experimental autoimmune encephalomyelitis mouse model of central nervous system demyelination. We determined that pEVs induced a spontaneous relapsing-remitting disease phenotype in MOG35-55-immunized C57BL/6 mice.

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Cellular senescence in progenitor cells contributes to diminished remyelination potential in progressive multiple sclerosis

Proceedings of the National Academy of Sciences

2019 Cellular senescence is a form of adaptive cellular physiology associated with aging. Cellular senescence causes a proinflammatory cellular phenotype that impairs tissue regeneration, has been linked to stress, and is implicated in several human neurodegenerative diseases. We had previously determined that neural progenitor cells (NPCs) derived from induced pluripotent stem cell (iPSC) lines from patients with primary progressive multiple sclerosis (PPMS) failed to promote oligodendrocyte progenitor cell (OPC) maturation, whereas NPCs from age-matched control cell lines did so efficiently.

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TIMP-1 Promotes Oligodendrocyte Differentiation Through Receptor-Mediated Signaling

Molecular Neurobilogy

2019 The extracellular protein tissue inhibitor of metalloproteinase (TIMP)-1 is both a matrix metalloproteinase (MMP) inhibitor and a trophic factor. Mice lacking TIMP-1 exhibit delayed central nervous system myelination during postnatal development and impaired remyelination following immune-mediated injury in adulthood.

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Long-Term Improvement of Neurological Signs and Metabolic Dysfunction in a Mouse Model of Krabbe's Disease after Global Gene Therapy

Molecular Theory

2018 We report a global adeno-associated virus (AAV)9-based gene therapy protocol to deliver therapeutic galactosylceramidase (GALC), a lysosomal enzyme that is deficient in Krabbe's disease. When globally administered via intrathecal, intracranial, and intravenous injections to newborn mice affected with GALC deficiency (twitcher mice), this approach largely surpassed prior published benchmarks of survival and metabolic correction, showing long-term protection of demyelination, neuroinflammation, and motor function.

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iPS-derived neural progenitor cells from PPMS patients reveal defect in myelin injury response

Experimental Neurology

2017 Primary progressive multiple sclerosis (PPMS) is a chronic demyelinating disease of the central nervous system (CNS) currently lacking any effective treatment. Promoting endogenous brain repair offers a potential strategy to halt and possibly restore neurologic function in PPMS. To understand how the microenvironment within white matter lesions plays a role in repair we have focused on neural progenitor cells (NPCs) since these are found in lesions in PPMS and have been found to influence oligodendrocyte progenitor cell maturation (OPCs).

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