CoNDA Research Project Leaders

The CoNDA Center supports junior faculty Research Project Leaders (RPLs). CoNDA RPL support consists of up to three years of direct research funding and structured mentoring, with the goal of helping the investigator successfully compete for R01-level independent research funding. Early Stage and New Investigators from the CoNDA's partnering institutions (UNMC, UNO, and Creighton) are eligible to apply when funding is available; the CoNDA supports between two and five RPLs at any given time, so calls for applications are intermittent. Join our mailing list and check our Funding Opportunities page to stay in the loop with our latest announcements.

Christopher Kovach, PhD

Investigating the Role of Attention in Perceptual and Cognitive Consequences of Parkinson’s Disease

Cognitive and emotional impairments are a significant source of morbidity in Parkinson’s disease (PD), beyond the hallmark motor symptoms; yet they remain a poorly understood aspect of the disorder. Among the significant and debilitating non-motor symptoms of PD are deficits in the perception of social cues, such as facial expressions of emotion. Perceptual deficits in PD might arise through several mechanisms, and as yet, no unified model of motor and perceptual symptoms has been convincingly demonstrated. Attention is crucial for the perception of complex stimuli; hence one possibility is that impaired perception in PD is a consequence of abnormal control of attention. Because eye movement is altered in PD in a manner consistent with other motoric changes, and because normal eye movement is closely linked to visuospatial attention, this possibility points to a common origin for attentional, perceptual, and oculomotor symptoms of the disorder. Attentional control is, moreover, an essential element of a wide range of cognitive processes, including working memory and executive function, raising the prospect of a more broadly unified model of cognitive and motor symptoms in PD, stemming from networks common to attentional and motor control. We propose a focused test of this theoretical perspective by examining whether and how abnormal eye movements in PD associate with impaired perceptual judgment of facial emotion, under the working hypothesis that impaired perception of facial expression will correlate tightly with abnormal patterns of gaze to faces. The opportunity to record from and stimulate structures targeted by therapeutic deep brain stimulation (DBS) will allow a detailed interrogation of the hypothesis and inform models of neural pathways governing attentional control. This combination of methods will allow the hypothesis to be tested across three levels of analysis: (1) through between-group comparisons of PD patients, matched comparison healthy subjects, and DBS patients treated for essential tremor (ET); (2) through within-group correlational analyses, afforded by the wide variability of non-motor deficits in PD; and (3) through within-subject comparisons across manipulations of DBS. Results of the study will inform future therapeutic strategies for cognitive symptoms of PD.

Christopher K. Kovach, PhD, is a systems and computational neuroscientist who joined the UNMC Department of Neurosurgery as a research faculty member in September 2023. Dr. Kovach decided to pursue a career in neuroscience research after completing undergraduate degrees in biology and physics at the University of Kansas and two years of medical school at the University of Iowa Carver College of Medicine. After finishing his PhD at the University of Iowa in 2008 and postdoctoral fellowships at Iowa and Caltech, he spent nine years as a research scientist in the Department of Neurosurgery at the University of Iowa Hospitals and Clinics, where he developed new methods of spectral analysis for brain signals, implementing them in publicly shared software packages.

Haiying Shen, MD, PhD

Modulating PNNs to Mitigate Epileptogenesis and Neurobehavioral Deficits in Mouse Models

Epilepsy is a brain disorder where seizures become frequent and long-lasting over time. While current medications can help control seizures, they do not stop epilepsy from developing, and their effectiveness often decreases with use. A key factor in this process is the breakdown of protective structures around brain cells called perineuronal nets (PNNs). These nets support specific brain cells that help keep brain activity balanced. However, during seizures, harmful enzymes break down PNNs, leading to increased seizure risk and cognitive problems. The Shen Lab's research aims to understand how PNNs influence epilepsy development and whether preserving them can prevent seizures from worsening. In his CoNDA Research Project, Dr. Shen will study (i) how PNNs change in different stages of epilepsy, (ii) how a key protein, OTX2, helps maintain PNN strength, and (iii) whether a safe, FDA-approved drug, dolutegravir, can protect PNNs and reduce seizures. By learning how to keep PNNs intact, we hope to develop new treatments that not only control seizures but also prevent epilepsy from progressing, improving the quality of life for people with epilepsy.

Dr. Haiying Shen, MD, PhD is an Assistant Professor in the Division of Pediatric Neurology at UNMC. He attended medical school and completed his residency at the Third Medical University in Chongqing, China, before completing a Fellowship at Boston University School of Medicine in Boston. Dr. Shen's research interests include exploring adenosine-based mechanisms in enurobehavioral disorders, studying treatment and prevention against epilepsy and its comorbidities, translational neuroscience, and adenosine manipulation in malignant tumors.

Eric Peeples, MD, PhD

Modulating 7-dehydrocholesterol to attenuate lipid peroxidation after hypoxic-ischemic brain injury

*pending NIH approval

Hypoxic-ischemic brain injury (HIBI) results in significant morbidity and mortality in more than 1.1 million infants per year worldwide. Despite available therapy, nearly half of infants who survive neonatal HIBI experience significant developmental impairment. Ferroptosis – a programmed cell death mechanism caused by phospholipid peroxidation – has recently been suggested to be a key mediator of cortical mitochondrial injury and hippocampal neuronal death after neonatal HIBI. Although early data support a significant role of ferroptosis in the pathophysiology of neonatal HIBI, the mechanisms of ferroptotic brain cell death after hypoxia-ischemia remain poorly understood and therapeutic targeting of ferroptosis in neonatal HIBI remains largely untested.
Recent studies suggest that 7-dehydrocholesterol (7DHC), which is an intermediary of the cholesterol biosynthetic pathway and the most oxidizable lipid in eukaryotes, plays a significant role in modulating lipid peroxidation. The accumulation of 7DHC in the membrane leads to increased 7DHC-derived oxysterols, decreased phospholipid peroxidation markers, and increased resistance to ferroptosis. Dr. Peeples' group has demonstrated that several commonly used FDA-approved medications (e.g., caripirazine, levetiracetam, and vitamin D) inhibit the enzyme 7-dehydrocholesterol reductase (DHCR7) and increase 7DHC levels. These observations serve as the basis to the overarching hypothesis of this proposal that administering 7DHC-elevating medications after neonatal HIBI will trigger an adaptive cellular response and attenuate ferroptosis-associated injury. To assess the ability of commonly used 7DHC-elevating medications to modulate ferroptosis and HIBI, Dr. Peeples plans to investigate the following specific aims: 1) elucidate the anti-ferroptotic mechanisms of 7DHC – including alterations to cell survival, lipid peroxidation markers, and the proteome – in an organotypic brain slice model; and 2) identify ideal dosing and short-term protective effects of 7DHC elevating medications in a mouse model of neonatal HIBI. Dr. Peeples proposes that 7DHC’s inherent redox chemistry allows it to fulfill a regulatory role in ferroptosis, likely through a “sacrificial” role, protecting against oxidation of other vital phospholipids and preventing cell death.

Dr. Peeples an associate professor in the UNMC Division of Neonatology and lead the Newborn Brain Injury Lab. His research is focused on understanding how early-life exposures shape neonatal brain injury, repair, and long-term neurodevelopmental outcomes. Using clinically relevant models, his work examines the cellular and molecular mechanisms underlying neonatal hypoxic-ischemic brain injury. Additionally, he is interested in investigating how genetic changes, medications, and other environmental exposures modify vulnerability and recovery in the developing brain.

Carlos Fernández-Peña, PhD

Elucidating the molecular and neural components of the C1→PAG and its contribution to Anxiety Disorders

*pending NIH approval

Anxiety disorders represent the most prevalent psychiatric conditions globally, yet their underlying neurobiological mechanisms remain insufficiently understood, limiting the efficacy of current treatments. This study identifies a novel role for a specific population of autonomic adrenergic neurons in the rostral ventrolateral medulla, termed C1 neurons, as a critical driver of anxiety-related behaviors. Preliminary data demonstrate that acute activation of C1 neurons, or their projections to the periaqueductal gray (PAG), produces long-lasting anxiety and aversion in mice. Conversely, inhibition of these neurons attenuates fear responses and prevents stress-induced anxiety. Using a multi-disciplinary approach including intersectional viral tools, single-cell RNA sequencing, spatial transcriptomics, in vivo calcium imaging, behavioral assays and machine learning this research aims to characterize the C1→PAG circuit by defining the molecular heterogeneity of C1 neurons and their functional synaptic connections. Furthermore, the study will map upstream interoceptive inputs to C1 neurons to understand how internal physiological signals contribute to the onset and chronification of anxiety states. Finally, the research will elucidate how the C1→PAG axis modulates activity patterns in the medial prefrontal cortex (mPFC) using 2-photon miniature microscopy to encode anxiety in health and disease. Together, these aims will provide a comprehensive molecular and circuit-level framework for understanding how adaptive arousal transforms into pathological anxiety. By uncovering the mechanisms of this brain-body hub, this work establishes a foundation for the development of targeted, more efficacious therapeutic interventions for anxiety disorders.

Dr. Fernández-Peña is an Assistant Professor in the Department of Neurological Sciences at UNMC. He received his PhD in neuroscience from the Universidad Miguel Hernandez in Spain, and completed his postdoctoral training at the University of Tennessee Health Science Center and St. Jude's Children's Research Hospital. His laboratory now focuses on elucidating the contribution of the body-brain connection to the onset and chronification of psychiatric illnesses, with the ultimate goal of advancing the development of more effective therapies.