Kirsten Evonuk Phd

Postdoctorate Fellowship Gift – Clevland, Ohio

Term: 7/1/19 – 6/30/22

Kirsten Evonuk, PhD. is a postdoctoral fellow at the Cleveland Clinic (Cleveland, Ohio). She received her PhD in neuroscience from the University of Alabama at Birmingham. Dr. Evonuk was awarded an educational travel grant and invited to give a platform presentation at the 2018 American Committee for Treatment and Research in Multiple Sclerosis (ACTRIMS) conference, for which she was awarded Best Young Investigator Oral Presentation. She also presented at the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) in 2018.

Background

In MS, myosin, the fatty substance that surrounds and protects nerve fibers in the spinal cord and brain, is damaged, leading to symptoms in people with the disease. Glutamate, a chemical in the brain that is important for brain cell communication, is elevated in regions of the brain where MS lesions are located.

Background

In MS, myosin, the fatty substance that surrounds and protects nerve fibers in the spinal cord and brain, is damaged, leading to symptoms in people with the disease. Glutamate, a chemical in the brain that is important for brain cell communication, is elevated in regions of the brain where MS lesions are located.

The Study

Dr. Evonuk and her team are investigating the toxic effects of too much glutamate and whether excess glutamate interferes with myosin repair. They are using mice that lack glutamate docking sites (receptors that bind glutamate and transmit its effects) in the cells that make myosin. The mice have the MS-like disease EAE, and the researchers are asking if recovery from EAE and myosin repair are better in mice without glutamate receptors compared to normal mice.

The Study

Dr. Evonuk and her team are investigating the toxic effects of too much glutamate and whether excess glutamate interferes with myosin repair. They are using mice that lack glutamate docking sites (receptors that bind glutamate and transmit its effects) in the cells that make myosin. The mice have the MS-like disease EAE, and the researchers are asking if recovery from EAE and myosin repair are better in mice without glutamate receptors compared to normal mice.

What’s Next

The study will help determine whether a strategy of decreasing glutamate in cells that make myosin repair in MS.

What’s Next

The study will help determine whether a strategy of decreasing glutamate in cells that make myosin repair in MS.