Kari Hoyt, Ph.D.

Associate Professor
College of Pharmacy

Degree: University of Pittsburgh

Contact Information
412 Riffe Building
496 W. 12th Avenue
Columbus, OH  43210
PHONE: (614) 292-6636
FAX: (614) 292-9083
E-MAIL: hoyt.31@osu.edu

Link to NLM PubMed publications list for Kari R. Hoyt (last 10 years)

Research Area:

Molecular mechanisms underlying the loss of neurons in neurodegenerative diseases.

Current Research:

Neuronal death or dysfunction is a consequence of acute events such as stroke or trauma, or more chronic degenerative processes that occur in Parkinson’s, Huntington’s, and Alzheimer’s diseases.  While the proximate trigger of neuronal death in these acute and chronic neurodegenerative processes may be different, it is becoming clear that the actual processes leading to death may be similar.  Our research is directed toward understanding the toxic cellular processes which lead to neuronal loss, with the ultimate goal of developing therapeutic interventions.  Calcium dysregulation, oxidative stress and mitochondrial dysfunction are among the causes often implicated in neuronal death, and are currently under study in the lab.

Currently, we are using Huntington’s disease (HD) as a model of chronic neurodegeneration.  HD causes damage to a particular brain region (the basal ganglia) resulting in difficulty controlling movement; the disease usually strikes in midlife.  HD has a specific genetic cause. Transgenic mice have been created which express the mutant HD gene and these mice develop brain damage and symptoms resembling the human disease.  This animal model of neurodegeneration is proving to be valuable in determining how the mutant protein causes neuronal dysfunction and ultimately cell death.  We study the pathology of HD in living cultured neurons expressing the mutant protein as well as the consequences of mutant protein expression in adult mice.  Since the mutant protein that causes HD is expressed in all cells, not solely neurons, we are also studying the consequences of mutant protein expression in non-neuronal tissue, particularly the heart.  Understanding how the mutant HD protein sensitizes cells to early death will facilitate the design of therapies for this disease, therapies that could be applied more broadly to other neurodegenerative diseases that share a common final mechanism of neuronal death.