Meet Our Scholars

The current Pepper Scholars are highlighted on this page. We are proud of their ambitious scholarship and high potential to shape the future of aging research.

Pepper Scholars are typically funded for at least two years to complete a research project. Select a name or scroll down to learn more about each scholar’s project.

Year One Pepper Scholars


Khanjan Shah, MD
Khanjan Shah, MD

Khanjan Shah, MD

Assistant Professor, Cardiovascular Medicine, Department of Medicine, College of Medicine

Project: “Examining the Co-Occurrence of Peripheral Arterial Disease and Alzheimer’s Disease and Related Dementias on Mobility, Falls, and Other Patient-Centered Outcomes in Older Adults”

About: Older adults with claudication – pain with exertion from peripheral arterial disease (PAD) – are at increased risk of falls and loss of independence. The additive impact of Alzheimer’s disease and related dementias (ADRD) on mobility, falls, and other patient-centered outcomes in patients with PAD is unknown despite representing a growing percentage of the aging population. Caregivers and physicians struggle to navigate crucial decision making in patients with PAD and ADRD because of a lack of information on outcomes in this population. This is particularly important because there are three potential treatment strategies for claudication – symptom control, catheter-based interventions (stents), and open surgery (bypass) – each with dramatically different treatment intensities and tradeoffs. Shared-decision making about ideal treatment strategy with patients and caregivers is not possible without information on patient-centered outcomes after each of the treatment options in specific

populations. Given the gap in knowledge of outcomes in patients with claudication and ADRD, the candidate proposes a “mixed-methods” study using the OneFlorida+ clinical research network with resources from the University of Florida Perioperative Cognitive Anesthesia Network (PeCAN) for ADRD. Aims 1 and 2 are retrospective analyses using real-world data to compare claudication treatment selection and resulting mobility-focused clinical outcomes in patients with and without ADRD. The candidate hypothesizes that patients with ADRD are more likely to have symptoms control and that they will have worse traditional and mobility outcomes

after open surgery. In Aim 3, the candidate will prospectively examine the neurocognitive profile of patients with claudication in order assess the hypothesis that there is a substantial portion of this group with undiagnosed cognitive impairment and disorders meeting ADRD clinical characteristics, co-occurring mood disorders, and frailty. A subaim is to assess caregiver burden in PAD patients with or without ADRD. These aims will be carried out by a multidisciplinary team with expertise in PAD, ADRD, large-dataset analyses, biostatistics, neuropsychology, geriatrics. This investigation will improve our understanding of patient-centered clinical outcomes for patients with PAD and ADRD. Data will be used to develop intervention strategies based on cognition, mood, and caregiver burden in order to improve mobility.

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Soamy Montesino Goicolea
Soamy Montesino Goicolea, MD

Soamy Montesino Goicolea, MD

Research Assistant Professor, Department of Community Dentistry and Behavioral Science, College of Dentistry

Project: “Deciphering the Neurobiological Role of Sleep Quality and Pain in Mobility Decline in Older Adults”

About: Building on an ongoing study funded by the National Institute on Aging (NIA), this research project aims to delve deeper into the intricate relationship between sleep quality, chronic pain, and the decline in mobility often observed in older adults. The parent study, which is designed to provide a comprehensive biopsychosocial profile of the elderly population and has already incorporated standardized measures of pain and mobility, provides a solid foundation for further exploration. In this ancillary study, we will supplement these existing measures with both objective and subjective sleep quality measures. A pioneering aspect of this study is the incorporation of a mobile Electroencephalography (EEG) technique, namely the EEG headband. This innovative approach enables an objective, ecologically valid evaluation of sleep in the comfort of the participant’s home. It also enhances our understanding of normal and pathological brain function, providing valuable insights into the neurological aspects of sleep, pain, and mobility. Our specific aims are twofold. Firstly, we aim to characterize the baseline pain and sleep measures that predict prospective mobility decline in aging. This will involve a detailed analysis of the data collected, identifying key indicators and trends that could signal a future decline in mobility. Secondly, we aim to investigate whether longitudinal changes in brain structure and function mediate the prospective association between sleep disorders and mobility decline in aging. This will involve sophisticated neuroimaging techniques and longitudinal data analysis, providing a deeper understanding of the neurological underpinnings of this association. By employing innovative techniques like the EEG headband, the study will underscore the combined impact of sleep quality and chronic pain on mobility. This comprehensive approach will allow us to examine the issue from multiple angles, ensuring a thorough and robust investigation. This research will provide essential preliminary data for a K23 application, facilitating the transition to independence for a clinically trained candidate.

The findings from this study will not only advance the candidate’s career but also contribute significantly to the field of geriatric research. In conclusion, this research project represents a significant step forward in our understanding of the complex interplay between sleep, pain, and mobility in older adults. The insights gained could have far-reaching implications for the treatment and management of these issues, ultimately improving the quality of life for older adults.

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Gene Crislip
Gene Crislip, PhD

Gene Crislip, PhD

Research Assistant Professor, UF Department of Physiology and Aging

Project: “High Salt in the Aged Kidney”

About: Chronic kidneys disease (CKD) is a major public health burden affecting nearly 37 million Americans and contributes to over $87 billion each year in Medicare costs. Aging is closely linked to renal pathophysiology, likewise, CKD is largely a disease of aging. Furthermore, both aging and CKD are associated with disruptions in circadian rhythms. Studies in this proposal will examine contributors to CKD progression in aged mice then determine if a circadian-based treatment therapy improves these outcomes.

High blood pressure is a major risk factor for CKD (www.cdc.gov/kidneydisease). There is an increased prevalence of hypertension and salt-sensitivity with aging.1 Similarly, expected changes occur within the kidney during aging that contribute to electrolyte abnormalities.2 Furthermore, inflammation increases within aging kidneys3. Studies outlined in this proposal will assess the fluid/electrolyte- and inflammatory-response to a high salt diet in young and old mice. Then, mice will undergo a time restricted feeding (TRF) regimen to determine if these responses to high salt are improved. There are reports of sex-specific disparities in both hypertension and electrolyte handling,4, 5 therefore, both male and female mice will be studied.

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Helena Zomer
Helena Zomer, PhD

Helena Zomer, PhD

Research Assistant Professor, UF Department of Physiological Sciences

Project: “A Regnerative Medicine Approach to Restore Estrogen Signaling in Older Adults’ Chronic Skin Wounds”

About: Debilitating non-healing wounds disproportionally affect older adults and lead to physical restrictions, social isolation, psychological distress, and loss of independence. Current treatments do not take into consideration the particularities of aged skin and often fail to restore tissue homeostasis. The age-associated 17β-estradiol (E2) deficiency plays a critical role in elderly impaired wound healing; however, there is still a critical knowledge gap on how to safely restore E2 signaling in the wounded skin. Given the progressive, degenerative effects of E2 deficiency, my research aims to test whether estrogen signaling can be modulated locally in chronic wounds of the elderly to promote robust healing using an unprecedented regenerative medicine approach. My objectives are to (1) understand the mechanisms of skin wound healing in older adults and (2) develop therapeutics leading to robust repair. My preliminary data indicates that an exosomal-enriched fraction (EEF) derived from the human placenta modulates E2 signaling in human and mouse skin cells and promotes wound healing in vitro (human cells) and in vivo (intact and ovariectomized mice). Strikingly, I found that EEF is enriched in multiple proteins involved in E2 signaling pathways and biosynthesis but contains only minimal amounts of E2 (~1 ng/ml). These findings suggest that novel regenerative medicine-based therapeutic strategies can be used to safely restore E2 signaling locally in elderly skin through paracrine stimulation of skin intracrine biosynthesis, and/or modulation of downstream targets of E2, avoiding deleterious systemic side effects of E2 replacement therapies. Using the system I developed as a tool, I will test my hypothesis that E2 signaling must be restored in elderly skin for optimal wound healing. My work proposes, for the first time, a link between the hallmarks of aging and age-associated estrogen deficiency and is expected to have a positive translational impact by pre-clinically establishing a novel strategy for improving skin wound healing in older adults.

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Year Two Pepper Scholars


Feng Yue
Feng Yue, PhD

Feng Yue, PhD

Assistant Professor, Department of Animal Sciences, University of Florida

Project: “Mechanisms of Sepsis-Induced Myopathy in Aging: Insights From a New Modified Surgical Sepsis Model by Single Cell Analysis”

About: Sepsis represents a major health problem for older adults. It is characterized by severe organ dysfunction and failure initiated by dysregulated host response to infection. While advances in critical care have allowed the number of older sepsis survivors to increase in the acute and subacute phases, many patients enter a state of chronic illness differentiated as the persistent inflammation, immunosuppression, and catabolism syndrome (PICS). Notably, ~75% of the surviving elderly patients suffer sepsis-induced myopathy, characterized by muscle wasting and weakness, eventually leading to disability and increased mortality. However, the mechanisms by which sepsis contributes to myopathy and persistent muscle dysfunction in older adults remain unknown. This represents a significant impediment to older adults’ independence, as well as a major knowledge gap in sepsis research and aging biology. Therefore, the central goal of this project is to identify the key sepsis-associated factors and cellular crosstalk mediating the sepsis-induced dysfunction of skeletal muscle in older adult hosts. We hypothesize that when faced with the severe immunological and systemic stress of sepsis, an aged host produces specific metabolite and signaling factors that communicate with muscle-resident cells to impair skeletal muscle function. Employing a novel murine model of surgical sepsis that better recapitulates human sepsis and PICS, we intend to determine the pathophysiological features of sepsis-induced myopathy in older adult septic mice. We hypothesize sepsis accelerates skeletal muscle and satellite cell dysfunction in aging (Aim 1). In addition, we will further employ comprehensive single-cell analysis to identify the intracellular cross-talks in skeletal muscle and the key regulatory factors underlying sepsis-induced myopathy in aging.

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