Jacob Ayers, Ph.D.

Assistant Professor

Department of Neuroscience
Center for Translational Research in Neurodegenerative Disease (CTRND)
1275 Center Drive
PO Box 100159
Gainesville, FL  32610-0159

Email:   jayers.123ja@ufl.edu
Phone: (352) 294-5159

Education:

2011-2015 Postdoctoral Fellow
Mentor: Dr. David Borchelt
Department of Neuroscience, University of Florida
Gainesville, FL
2010-2011 Research Associate
Mentor: Dr. Anthony Kincaid
Creighton University
Omaha, NE
2010 Ph.D.
(Medical Microbiology & Immunology)
Creighton University
Omaha, NE
2004 B.S.
(Microbiology)
University of New Hampshire
Durham, NH

Research Summary:

I began work in the prion field studying the mechanisms that govern prion strain targeting by examining the in vivo properties of several hamster-adapted prion strains. Using sciatic nerve or intracerebral inoculation to introduce these pathogens, I observed that the different clinical symptoms and incubation periods observed among the strains were not due to hypothesized differences in neuroanatomical transport or neuronal susceptibility, but to the strain-encoded relationship between PrPSc replication, stability, and processing in neurons. These studies provided the prion field with a wealth of information regarding these particular prion strains and helped to better understand what accounts for their unique pathogenicity.

Using the knowledge and techniques learned from the studies listed above, I began investigating the potential prion-like properties of SOD1. My studies were the first that examined these properties in vivo. We revealed the permissiveness for the G85R-SOD1:YFP mouse model for MND transmission through the administration of misfolded SOD1 preparations including spinal cord homogenates from paralyzed mice and recombinant SOD1 protein. Using this model we have gone on to demonstrate the ability for SOD1 pathology to be induced locally and spread to synaptically linked populations of neurons. These novel findings describe a number of prion-like properties inherent of the SOD1 protein and describe a unique mouse model and injection paradigm that result in a spreading symptomology that mirrors that observed in ALS patients.

 

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