FacultyJonathan Fox

Graduate Neuroscience Program

Associate Professor, Department of Veterinary Science



Welcome! My lab at the University of Wyoming studies mechanisms of Huntington's disease using mouse models. We have several ongoing projects that use interdisciplinary approaches to seek and develop disease modulating interventions that may be translatable to human HD. I also have veterinary diagnostic responsibilities within the Department of Veterinary Sciences. Thank you for taking an interest in our work. Please contact us if you have any questions.

About Huntington's Disease

Huntington's disease (HD) is a genetic, neurodegenerative disease that effects about 30,000 people in the United States. Patients diagnosed with Huntington's experience involuntary movements (chorea), psychiatric disturbances and cognitive decline. HD is caused by a CAG repeat expansion within the huntingtin gene that results in a polyglutamine expansion within the encoded protein.  The normal htt gene contains less than 35 CAG repeats. Expansion of CAG repeats beyond this gives rise to HD with close to 100% genetic penetrance.  The disease process targets primarily the cerebral cortex and neostriatum where there is degeneration and loss of neurons.  Research efforts by many groups over the last several years has led to tremendous advances in understanding HD pathogenesis.  This new understanding is helping to advance the development of therapies to treat HD.



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About Dr. Fox

About Dr. Fox >

We're hiring!

The Fox Lab is looking for a graduate student ( PhD) and motivated undergraduate students to join the research group. Interested individuals should contact Dr. Jonathan Fox.

Research Projects

Iron metabolism

One of the primary projects in my lab is the study the impact of dietary iron on progression of HD. This collaborative project explores mechanisms of brain iron homeostasis dysregulation in HD models.  Appropriate manipulation of brain iron could provide therapeutic benefit in HD. We have published data demonstrating that neonatal administration of iron exacerbates HD symptoms and are currently completing studies to elucidate the mechanism underlying this finding.

Iron Publications

Amyloid Precursor Protein Haploinsufficiency Preferentially Mediates Brain Iron Accumulation in Mice Transgenic for the Huntington's Disease Mutation

Impact of high iron intake on cognition and neurodegeneration in humans and in animal models: a systematic review

Neonatal iron supplementation potentiates oxidative stress, energetic dysfunction  and neurodegeneration in the R6/2 mouse model of Huntington's disease.

Neonatal Iron Supplementation Induces Striatal Atrophy in Female YAC128 Huntington's Disease Mice

Iron accumulates in Huntington's disease neurons: protection by deferoxamine.

Neuroinflammation and chronic infection

We are involved in a collaboration with Dr. Jason Gigley, an immunologist in the Department of Molecular Biology at the University of Wyoming. The goal of this collaboration is to study the role of the immune system, and specifically neuroinflammation, on HD processes. One aspect of this project is to study the impact of chronic infection by the parasite, Toxoplasma gondii, on HD.

Neuroinflammation Publications

Huntingtons Disease Mice Infected with Toxoplasma gondii Demonstrate Early Kynurenine Pathway Activation, Altered CD8+ T-Cell Responses, and Premature Mortality.

Environment and mouse models

We are also interested in how other environmental factors, such as selenium, influence HD. In addition, we use mouse models of HD and it is important to fully understand and characterize these models. Some of our work has contributed to understanding these mouse models.


Altered selenium status in Huntington's disease: neuroprotection by selenite in the N171-82Q mouse model.

Thiol-disulfide Oxidoreductases TRX1 and TMX3 Decrease Neuronal Atrophy in a Lentiviral Mouse Model of Huntington's Disease.

Characterization of Striatal Neuronal Loss and Atrophy in the R6/2 Mouse Model of Huntington's Disease.



1R56NS097813-01A1: Environmental and Mutant Huntingtin-mediated Upregulation of Indoleamine-2,3-dioxygenase in Huntington's Disease Pathogenesis


5R01NS079450-02: Defining the role of brain iron dysregulation in Huntington's disease 

5P30GM103398-03: Interaction between neuroinflammation and neurodegeneration using latent Toxoplasma gondii infection in a mouse model of Huntington's Disease (Pilot Project under University of Wyoming P30 Center Grant)

5R21NS072372-02: Oxidation-dependent mutant huntingtin oligomers and Huntington's disease pathogenesis

5P20RR015640-10: Neuronal Iron in Huntington's Disease 


Neuroanatomy for medical students, WWAMI program
Diseases of Food Animals and Horses 

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