Research Laboratories

Alzheimer's Disease and Cognition

Principal Investigator:  Huntington Potter, PhD
E:   |   P:   303-724-7385

For details of these laboratory studies, visit this link.

  • Exploring the Mechanism of Action of GM-CSF (Leukine®) in Alzheimer's Disease
  • Investigating Type 2 Diabetes in Alzheimer's Disease
  • Understanding Chromosome Mis-segregation in Alzheimer's Disease and Other Neurodegenerative Disorders
  • Understanding the Role of ApoE in Alzheimer's Disease
  • Environmental Enrichment, Exercise, and Rolipram Studies
  • Caffeine and Melatonin Studies


CU Neuro-Magnetic Laboratories

Principal Investigator:  Isabelle Buard, PhD
Laboratory:  303-724-8655
TMS Laboratory:  303-724-2205

Our laboratory supports magnetoencephalography (MEG) and transcranial magnetic stimulation (TMS) research and clinical services for the greater Denver area. Our interdisciplinary team is dedicated to advancing the use of MEG and TMS in diagnostics and treatments for neurological conditions.

For details, visit this link.

Neuroimmunology: Autoimmune Inflammatory Disorders of the Central Nervous System

Principal Investigators:  Jeffrey L. Bennett, MD, PhD and  Gregory P. Owens, PhD  
E:  E:   |   P:   303-724-4314

Our laboratories investigate the direct and downstream pathways leading to CNS damage in the neuro-inflammatory diseases: multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and myelin oligodendrocyte glycoprotein associated disease (MOGAD). We focus our efforts on the role of B cells and their antibody products in initiating CNS damage, disrupting the blood-brain barrier and interfering with CNS repair. Utilizing recombinant monoclonal antibodies cloned from expanded plasmablasts infiltrating the CNS in NMO and MS patients, we have developed both in vivo and ex vivo models that recapitulate important pathologic features of each disease, developed novel animal models for the study of disease-specific pathology, autoantibody transit across the blood-brain barrier (BBB) and the molecular interactions between antibody Fc regions and complement. Using pathogenic myelin-specific rAbs from MS patient CSF B cells that cause extensive complement-mediated oligodendrocyte loss and demyelination, we have developed novel models of MS lesion formation and are actively investigating the mechanisms the drive lesion formation and repair using advanced techniques in immunology, cell biology, and genomics. Ongoing collaborative studies with Drs. Wendy Macklin and Ethan Hughes in the Department of Cell and Developmental Biology are focused on defining the molecular mechanisms through which microglia regulate oligodendrocyte maturation and CNS remyelination.

In addition, our laboratory directs translational research activities in MS, NMOSD, MOGAD, and autoimmune encephalopathies. Research involves the collection and analysis of PBMCs, serum, plasma, and cerebrospinal fluid from affected patients.

Select Publications-Bennett, JL and Owens, GP

Neurovirology: Role of Varicella Zoster Virus in the Central Nervous System

Principal Investigator:  Maria A. Nagel, MD  
E:   |   P:   303-724-4326

For details of these laboratory studies, visit this link.

  • COVID-19 Inflammatory Response
  • Varicella Zoster Virus (VZV) and Stroke
  • Varicella Zoster Virus and Other Inflammatory Manifestations
  • Varicella Zoster Virus, Amyloid-Beta, Amylin, and Amyloid
  • Development of Antiviral Nanoparticles Using a Guinea Pig Model of VZV Infection
  • Development of Induced Pluripotent Stem Cell-Derived Motor Neurons to Study Viral Motor Neuron Disease
  • Herpesvirus Infection and Cognitive Impairment
  • Neurokinin-1 Receptor Antagonists to Treat VZV Central Nervous System Disease

CV-Nagel, M

Neurovirology: How Common Viruses Can Lead to Stroke and Neurodegeneration

Principal Investigator:  Andrew Bubak, MS, PhD 
E:   |   P:   303-724-0204

Our laboratory focuses on studying the mechanisms in which varicella zoster virus (VZV) and herpes simplex virus (HSV-1) can induce stroke and neurodegenerative diseases. We use state-of-the-art technologies such as spatial transcriptomics and proteomics, single-cell sequencing, and multi-probe electrophysiological recordings of free-roaming mice. Specific areas of research currently being conducted:

  • Non-infectious VZV exosomes and central nervous system vulnerability
  • Non-infectious VZV exosomes and longitudinal stroke risk
  • Alphaherpesviruses and Alzheimer’s disease progression
  • VZV and diabetes onset
  • VZV and motor neuron diseases

CV-Bubak, A

Neurovirology: In Vivo Models of Varicella-Zoster Virus Neurotropism

Principal Investigator:  Ravi Mahalingam, PhD  
E:   |   P:   303-724-4324

Our laboratory studies varicella virus pathogenesis and neurological manifestation of varicella reactivation including multi-organ disease. Our studies explore the role of cell-mediated immunity in the regulation of varicella latency and reactivation using simian varicella virus infection in non-human primates as a model. We use state-of-the-art technologies such as PCR, infectious BACMID, CRISPR, flow cytometry and in situ methods to understand the state of varicella virus infection in multiple tissues.


Neurovirology: Virus Infections of the Central Nervous System

Principal Investigators:  Kenneth L. Tyler, MD and Penny Clarke, PhD
E:   E:   |   P:   303-724-4344

Role of Microglia in West Nile Virus (WNV) Infections of the Central Nervous System (CNS)
Microglia are the resident immune cells of the CNS, and microglial activation is a key cellular response to CNS disease states, including infections, inflammation, trauma, cancer, and degenerative conditions such as Alzheimer's disease and multiple sclerosis. We have demonstrated that WNV infection of the CNS results in a robust activation of microglia and that deletion of microglia enhances disease severity. Current studies will determine the mechanism by which microglia protect the host from WNV-induced CNS disease.

Identification of Enterovirus D68 (EV-D68) as the Cause of Acute Flaccid Myelitis (AFM)
n 2014, the United States (U.S.) experienced an unprecedented epidemic of EV-D68-induced respiratory disease that was temporally associated with the emergence of acute flaccid myelitis (AFM), a paralytic disease occurring predominantly in children. Although a causal link between EV-D68 infection and AFM has not been unequivocally established, clinical, immunological, and epidemiological evidence points to EV-D68 as the causative agent. We have shown that clinical isolates of EV-D68, from the 2014 outbreak, cause CNS disease in neonatal mice that has a striking resemblance to the AFM. In ongoing studies, we will identify genetic factor(s) that have increased EV-D68 neurovirulence and will define specific mechanisms by which EV-D68 causes CNS disease.

Novel Treatments for Viral Infections of the CNS
We will utilize EV-D68- and WNV-infection of mice and ex vivo brain and spinal cord slice cultures to evaluate novel treatments for viral infections of the CNS. Examples include antivirals, such as telaprevir and its derivatives, human-derived monoclonal antibodies, and the microglial stimulant
Granulocyte-macrophage colony-stimulating factor (GMCSF).


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