National Research Service Award F30 for Dr. Kellogg
Collyn Kellogg, Ph.D. have received a Ruth L. Kirschstein National Research Service Award (NRSA – F30) Fellowship for M.D./Ph.D. training. His project – ‘Regulation of Microglial Function by Major Histocompatibility Complex I in Aging and Alzheimer’s Disease’ will support the completion of his Ph.D. research and M.D. training. Specifically, his project will examine the hypothesis that the increased expression of Major Histocompatibility Complex-I and their receptors is a mechanism through which microglia can signal cell-autonomously to themselves or cell-non-autonomously to other microglia to induce phenotypic switching to a more reactive phenotype. This is one of only five F30 fellowships to be awarded in Oklahoma in the past decade.
VA Pilot Award to Study Traumatic Brain Injury
The OKC VAMC has awarded Dr. Kellogg a VA Pilot Project that examines blast traumatic brain injuries. We have developed a shock tube that uses pressurized air to create a pressure shock wave similar to that which may be experienced by service members in combat. Our methods allow us to vary the intensity to investigate the impact of different injury levels. The funds will support the technician, Hannah Ray, working on the project, as well as some of the mouse colony, RNA isolation, and downstream analysis. We will cause different intensities and frequencies of TBI and follow how long the impacts of blast injury are evident through behavioral studies and RNA, specifically focusing on microglia. Our goal is to elucidate the short term and persistent changes in glial cells following blast traumatic brain injury. We hope this project extends the understanding of the pathophysiology of persistent brain damage following traumatic brain injury and opens avenues for novel interventions that can improve the neuronal landscape post-TBI by modulating the microglial response.
New NIH grant to study mechanisms of eye aging
Drs. Chucair-Elliott and Freeman have received a new award from the National Eye Institute. Aging is the principal risk factor for age-related macular degeneration (AMD), a neurodegenerative disease characterized by the irreversible loss of vision. Atrophy of the retinal pigmented epithelium (RPE) layer is an AMD hallmark that precedes photoreceptor cell loss. However, the mechanisms underlying RPE impairment with aging and exacerbation by poor diet are unclear. Epigenetic processes (DNA modifications and chromatin accessibility) in the RPE may play a central mechanistic role in the pathogenesis and progression of AMD. These studies will examined changes in RPE mC/hmC and chromatin accessibility patterns with aging, RPE-specific differential changes in the translatome, and interrogate the potential of Western and ketogenic dietary patterns, in combination with impaired oxidative stress resolution pathways, to exacerbate or ameliorate changes in the RPE epigenome and gene expression profiles.