2016 MBI Fellowship awardees announced

Published: September 22nd, 2016

Category: Awards

The MBI Fellowships were established to support students and fellows conducting neuroscience and brain-related research in MBI-affiliated labs.

This year’s awardees:

Sarah A. Johnson, postdoctoral associate in the department of neuroscience

$60,000 over two years

Mentor: Sara Burke, Ph.D.

Project: Among the symptoms of age-related cognitive decline is a decreased capacity for distinguishing between similar events. This aspect of memory is supported by stimulus discrimination abilities, which are consistently impaired in older adults. The goals of Johnson’s research are to identify the neuronal mechanisms that are responsible for stimulus discrimination deficits in aged animals, and determine how these mechanisms contribute to memory loss. She has developed and validated rodent stimulus discrimination tasks in which aged rats show deficits that directly parallel those observed in humans. Ongoing studies employ high-density multi-site in vivo electrophysiological recordings to pinpoint age-related changes in the activity of single neurons during discrimination tasks. Complementary mapping of neuronal gene expression in cortical and hippocampal regions will establish how aging alters the representation of similar stimuli across brain circuits.

Changjun Yang, post-doctoral associate in the department of neuroscience

$30,000 over two years

Mentor: Eduardo Candelario-Jalil

Project: Stroke is a leading cause of mortality and long-term disability in adults. Only a small percentage of stroke patients reach a hospital early enough to receive tissue plasminogen activator (tPA) treatment, the only FDA-approved therapy. Thus, development of novel therapeutic strategies is urgently needed to reduce brain damage after stroke. Adropin is a recently identified polypeptide that is abundantly expressed in brain and liver and has been shown to reduce endothelial dysfunction and insulin resistance. However, little is known of the effect of adropin in the brain and whether this polypeptide mediates neuroprotection in ischemic stroke. Recent findings from our lab revealed that the gene encoding for adropin, Enho, and protein levels in brain were significantly decreased in rats and mice following ischemic stroke, which were associated with increase in adropin levels in plasma. Importantly, we also found a dramatic increase of adropin levels in stroke patients within six hours after the symptoms onset and the plasma adropin levels remained elevated in convalescent stroke patients at three days when compared with non-stroke controls. These preliminary data strongly suggest that increased adropin in blood may serve as a novel biomarker of acute stroke and maintaining adropin levels in the brain may be of potential value to reduce stroke injury. The long term goal of the current study is to determine the neuroprotective role of adropin in ischemic stroke and explore the underlying mechanisms of its protection. It is our expectation that this proposed research will ultimately contribute to the development and validation of adropin as an effective neuroprotective strategy in the treatment of ischemic stroke.

Marissa Ciesla, pre-doctoral student in the College of Public Health and Health Professions

$30,000 over two years

Mentors: Gordon S. Mitchell, Ph.D., and Dr. Elisa Gonzalez-Rothi, DPT, Ph.D.

Project: Injury to the cervical spinal cord (SCI) disrupts descending projections from brainstem respiratory centers to spinal motoneurons, resulting in paralysis of respiratory muscles and ventilator dependence. Respiratory insufficiency is the leading cause of morbidity and mortality following cervical SCI. Folate (folic acid, vitamin B9) facilitates neural tube closure and reduces the incidence of fetal malformations. The role of folate in the adult CNS is far less clear. Evidence suggests that folate may minimize neuronal injury, enhance neuronal regeneration and improve functional recovery after injury to the central nervous system through DNA methylation and by mitigating oxidative stress, apoptosis and inflammation. The impact of folate supplementation on functional recovery of breathing capacity following SCI has not been investigated. Interestingly, persons with SCI report reduced dietary intake of folate by as much as 75 percent, suggesting that folate supplementation may be a potential therapeutic target. Repetitive acute intermittent hypoxia (rAIH) is another therapeutic tool that has shown tremendous promise to restore both respiratory and somatic motor function following cervical SCI. The impact of folate on rAIH-induced respiratory motor recovery and/or axonal sprouting/regeneration following incomplete SCI has not yet been investigated. The goals of this project are to test the hypotheses that folate: 1) mitigates breathing deficits following cervical SCI either by preserving and/or restoring lost respiratory motor function, and 2) further enhances rAIH-induced respiratory motor recovery and axonal sprouting/regeneration. Both folate supplementation and rAIH have been shown to be safe in humans; thus, if successful, this project will advance clinical approaches for treating respiratory dysfunction and promoting plasticity following cervical SCI.