Past Students

Linda D'Silva Pic

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Linda D'Silva 
Grad Student, Department of Rehabilitation Science


Project Title: To study the impact on the vestibular system in type 2 diabetes and acute concussion

Research Mentor: Patricia Kluding
Co-Mentor: 
Hinrich Staecker

The human vestibular system plays an important role in gaze stability and maintenance of balance. The peripheral sensory apparatus of the vestibular system comprises of the semicircular canals and otoliths which are motion sensors. While the semicircular canals detect angular acceleration; the otoliths play an important role in detecting linear acceleration.  Both sensory organs are damaged by various disease processes; both acute and chronic in nature. The main purpose of my study is to compare the effect of two distinct disease processes on the peripheral vestibular system, specifically the otolith organs. I will study how type 2 diabetes, a chronic condition, and an acute injury like a concussion affect the otoliths. Once that baseline information is collected, I will look at specific interventions to rehabilitate the otolith organs in the peripheral vestibular system and assess how the two disease states respond to vestibular rehabilitation.

Sarah Dominguez Pic

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Sarah Dominguez
Grad Student, Department of Anatomy and Cell Biology

Project Title: Explanation of Pain and Central Sensitization Can Improve Symptoms and Restore Function in Chronic Pelvic Pain

Research Mentor: Wen Liu, PhD
Co-Mentor: TBA

Sarah has practiced as a physical therapist clinically for 9 years, 8 of these specifically in women’s health relating to pelvic dysfunction in all phases of women’s lifespan. She has recently added lymphedema and a new found interest in oncology rehabilitation, seeing more patients with chronic pain, or movement dysfunction due to the sequeulae that follow cancer treatment. The cancer population is understudied, especially female cancers of the pelvic region.  Cancer treatment can lead to nerve damage, lumbar spine and hip movement dysfunction, pelvic pain syndromes, incontinence and lymphedema. Sarah has treated pelvic pain and incontinence for years, but has recently seen an increase in referrals for women who have chronic pelvic pain as a result of surgery or radiation or both.  It is well established that pelvic pain can impact a person’s life, work, interpersonal relationships as well as mental health.  This population is under-represented in the literature however, regarding neurological dysfunction and how this applies to our rehabilitative approach to these patient populations. Uncovering whether the painis more centrally or peripherally mediated and whether loss of spinal inhibition plays a role in post-cancerchronic pelvic pain,will be important in devising optimal rehabilitation therapies.


Natalia Loskutova Pic

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Natalia Loskutova, MD
Grad Student, Department of Physical Therapy and Rehabilitation Sciences

Project Title: Brain atrophy as a mechanism of bone loss in Alzheimer's disease

Clinical Mentor: Jeffrey Burns
Research Mentor: John Stanford

Description: Epidemiologic projections indicate that the prevalence of Alzheimer’s disease (AD) will increase dramatically in the coming decades due largely to the demographics of the disease and our aging population. Associated cognitive and physical decline greatly contributes to disability in older adults and places considerable burden on the health system, patients, and caregivers. Bone health is an important issue in AD given that AD patients are at higher risk than cognitively healthy adults for osteoporosis, falls, bone fractures and poor post-fracture outcomes.  Bone mineral density (BMD) is a strong predictor of bone fractures and accounts for 60-70% of bone strength. The central nervous system (CNS) plays a direct role in regulating bone remodeling, primarily through the actions of the hypothalamus.

Clinical, neuropathological, and neuroimaging data together suggest that the hypothalamus is affected in AD and undergoes neuronal loss, profound plaque and tangle formation and overall atrophy. However, there have been no studies to investigate whether neurodegeneration of CNS, and the hypothalamus specifically, is associated with bone loss. Thus, the overall hypothesis of my research project is that atrophy of the hypothalamus and loss of hypothalamic neurons associated with AD may be one of the mechanisms of accelerated bone loss in AD. The aim of my study is systematic evaluation of bone health in AD and exploration of underlying neural substrate of an association between BMD and neuroimaging markers of neurodegeneration (i.e. global and regional measures of brain volume) in early AD and non-demented aging.

Stefanie Kennon-McGill Pic

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 Stefanie Kennon-McGill

Grad Student, Department of OtolaryngologyProject Title: The role of spontaneous neural firing in an animal model of tinnitus.Research Mentor:  Dianne Durham
Co-Mentor: Hinrich Staecker

Tinnitus, or ringing in the ears, is a common condition affecting many older individuals as well as military personnel. Although it affects many people worldwide, the causes of tinnitus are not yet well known, therefore making it difficult to provide adequate rehabilitation and treatment for tinnitus sufferers. It is widely believed that when the peripheral auditory system is damaged, deafferentation occurs in the central auditory structures, leading to an imbalance of excitatory and inhibitory input. This imbalance may cause a change in spontaneous neural activity and thus cause the perception of tinnitus. My research focuses on the spontaneous neural activity specifically in the inferior colliculus following acoustic damage to the auditory system. This research will allow for further insight into the mechanisms of tinnitus, and perhaps contribute to the future development of treatments and rehabilitation for individuals experiencing tinnitus.

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Anna Mattlage
Grad Student, Department of Physical Therapy and Rehabilitation Science

Project Title: The role of exercise on inflammatory biomarkers and IGF-1 levels following an acute stroke.Research Mentor:  Sandra Billinger
Co-Mentor: Doug Wright

Description: Stroke is the leading cause of death and disability for older adults in the United States with approximately 795,000 new or current strokes occurring each year.  New and innovative intervention strategies that mitigate disability and improve functional outcomes are essential for improving the lives of stroke survivors.  People after stroke who have lower levels of inflammation and higher serum values of insulin-like growth factor 1 (IGF-1) have been shown to have better outcomes.  Furthermore, exercise is a potent stimulus that may facilitate a reduction in inflammation and improve circulating IGF-1 levels following stroke.  The goals of this project are to: 1) characterize the effects of exercise on circulating levels of inflammatory markers and IGF-1 and 2) determine whether exercise initiated during the acute stage of recovery demonstrates neuroprotective effects and improves neurorehabilitation outcomes.  This project could have a significant impact on the therapeutic effects of exercise in clinical practice, rehabilitation research, and improve quality of life for the survivors of stroke.

William Messamore Pic

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William Messamore
Grad Student, Department of Molecular and Integrative Physiology

Project Title: Cortical Control of Hindlimb Muscles

Research Mentor: Paul Cheney
Co-Mentor: Jules Nazzaro

Description: Cortical organization relates directly to aspects of movement disorders, making understanding normal cortical organization and control of movement a topic of clinical and rehabilitative importance. The cortical control of the arm and hand in primates has been studied extensively; however, there have been only a handful of studies focusing on the control of the lower limb. Recent research in our lab has elucidated the basic features of the M1 cortical hindlimb map along with the strength and nature of the synaptic linkages. I plan to determine the characteristics of M1 cortical output effects on ipsilateral hindlimb muscles, in comparison to effects on the contralateral side. In addition I plan on using electrophysiological recording techniques to determine the organization of output effects from single M1 cortical neurons to hindlimb muscles including fast and slow ankle extensor muscles. The data collected from these experiments will form the foundation for interpreting data from future experiments designed to investigate recovery of lower extremity function following brain injury.

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Kristin Russell
Grad Student, Department of Pharmacology, Toxicology, & Therapeutics

Project Title: Functional and biochemical effects of brain fatty acid content on recovery from juvenile TBI

Research Mentor: Beth Levant
Co-Mentor: Russell Swerdlow

Description: Children under 5 years of age are at high risk for sustaining traumatic brain injuries (TBI) and tend to have poorer outcomes despite the greater neuroplasticity in children. Omega-3 polyunsaturated fatty acids (PUFA), a major component of neural membranes, accumulate in the brain during late gestation and early childhood. Low dietary content of these essential fatty acids results in decreased omega-3 PUFA accumulation in the developing brain. Omega-3 PUFAs have multiple neuroprotective and anti-inflammatory activities, thus low dietary omega-3 PUFA content may put children at risk for poorer outcomes after TBI. Therefore, my research focuses on how the functional and biochemical outcomes of juvenile TBI are influenced by the fatty acid composition of the brain. Additionally, I am researching the possibility of using omega-3 fatty acids as a therapeutic after TBI to decrease inflammation and apoptosis and improve outcomes. Knowing the full relationship between omega-3 PUFAs and brain injuries could lead to novel therapeutic strategies to improve the outcomes of TBI.

 Matt Stroh Picture

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Matt Stroh
Grad Student, Neuroscience


Project Title: Understanding the role of iron homeostasis and mitochondrial function in a mouse model of neurodegenerative disease and diabetesResearch Mentor: Hao Zhu
Co-Mentor: Doug Wright

Alzheimer's disease can be characterized by a gradual decline in cognition and the ability to perform daily functions such as task planning and speaking. Mounting evidence suggests that mitochondrial function plays a large, if not central, role in Alzheimer's and other neurodegenerative diseases. Interestingly, a diet high in medium chain triglycerides (fats) and low in both protein and carbohydrates (ketogenic diet) has been shown to improve symptoms in neurodegenerative conditions such as Alzheimer's disease and Parkinson's disease.  This is interesting in that ketone bodies are a preferred source of fuel for the brain, strongly implicating a role for mitochondrial function and metabolism in the pathogenesis of these diseases.  I have designed and begun work on a minor project that aims to help elucidate the role of electron transport chain (ETC) dysfunction in brain aging and neurodegeneration.  I am utilizing a previously described, endogenous pathway to deliver exogenous, engineered transcripts to mitochondria in a brain specific manner.  These transcripts serve as either non-coding, anti-sense RNAs targeted against mitochondrial transcripts that act as translational blockers/terminators resulting in decreased availability of critical ETC components (namely Complex I and Complex IV), or functional mRNAs encoding mutated or otherwise dysfunctional ETC subunits. The novelty behind this approach is the ability to localize and translate exogenous transcripts in mitochondria.  Since cytosolic expression of mitochondrial encoded subunits fails to result in functional incorporation into the ETC, this approach will allow the analysis of controlled disturbance of electron transport chain activity and its effect on synaptic plasticity and neural viability.

In parallel, I have begun work on a major project that aims to identify the role that Ncb5or, a novel oxidoreductase, plays in altered iron metabolism and dyshomeostasis in neurodegenerative diseases.  Diseases such as Friedreich's ataxia exhibit many of these same characteristics, including a 30% diabetes incidence amongst patients and significant defects in iron metabolism and iron-sulfur cluster processing, resulting in iron accumulation in mitochondria. Ncb5or has been shown to play a critical, albeit uncharacterized, role in iron metabolism/homeostasis in mice.  Global knockout mice rapidly develop lean diabetes and exhibit cognitive, behavioral, and neuromuscular junction defects at an early age, prior to the onset of diabetes.  Also, significant changes in electron transport chain complex levels accompany a drastic change in mitochondrial respiratory rate and oxygen consumption.  I am currently working with a brain-specific Ncb5or knock-out mouse that results in a functionally inactive form of Ncb5or in the brain. Preliminary data suggest that these mice exhibit the same defects seen with the global, non-diabetic knockout mice as well as other uncharacterized phenotypes. One significant benefit of the brain specific knockout model is that of lifespan. Global knockout mice rapidly develop diabetes and die at a relatively young age (20 weeks in males). It is critical to work with a model that will allow us to evaluate the neurological deficits that progress with age. Unfortunately, treatment for Friedreich's ataxia associated neurological deficits is limited to symptom maintenance and slowed disease progression, involving physical therapy sessions with low resistance training and gait training using visual cues.  While such methods have proved successful in temporarily improving quality of life and slowing disease progression, no therapy or target has been identified that can halt disease progression all together. Understanding the role of Ncb5or in iron processing and neurodegenerative diseases might help to identify pathways or processes that are potential targets for therapeutic intervention.

 Jessica Witherspoon Picture

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Jessica Witherspoon
Grad Student, Physical Therapy and Rehabilitation Service

Project Title: Glenohumeral Joint Laxity: A Neural Contribution

Research Mentor: Terence McIff
Co-Mentor: Irina Smirnova

Description: The purpose of this study is to assess neural density and collagen composition of the glenoid labrum and capsule as they relate to anterior and posterior shoulder laxity. When reduced glenohumeral joint (GHJ) stiffness occurs, GHJ laxity increases resulting in shoulder instability, which can progress to subluxation and dislocation. According to research, the occurrence and reoccurrence of subluxations and dislocations become career ending for the workforce as well as for athletes. Rehabilitation and surgery protocols have been established to address instability related to GHJ dynamic stabilizers (musculature); however, there is a 14-94% reoccurrence post rehabilitation and/or surgery. This study will investigate the properties of the glenoid labrum and capsule, which are static stabilizers, as they relate to GHJ laxity and stiffness. It is hypothesized that the shoulders with a larger laxity zone and less tissue stiffness will present with lower neural densities as well as lower type I (providing tensile strength) to type III (sustaining elasticity) collagen ratios. The specific aims of this study are: 1) to define anterior and posterior GHJ instability based on the analysis of stiffness and zone of laxity in cadaveric models without muscular involvement; 2) to identify neural density in the labrum and capsule and determine whether it correlates with GHJ laxity; and 3) to determine whether the ratio of type I to type III collagen in the glenoid labrum and capsule correlates with GHJ stiffness. The clinical load and shift stability test will be performed on fifteen cadaveric shoulder pairs in the sagittal plane by a physical therapist and the Instron material testing machine to establish the zone of laxity and stiffness. Samples will then be collected from the anterior, anteroinferior, posterior and posteroinferior aspects of the labrum and capsule to evaluate the neural density of pacini and ruffini corpuscles as well as golgi tendon organs. In addition, the type I to type III collagen ratio will be determined. From these data, labral and capsular proprioceptive properties and stiffness will be correlated with available anterior and posterior joint movement for each shoulder. Determining the neural density, using immunofluorescence, will allow recognition of proprioceptive contribution to GHJ stability. Evaluating type I to type III collagen protein ratio, using enzyme-linked immunoassay (ELISA) will implicate the extent of tensile strength available to limit joint movement. We expect the shoulders with larger laxity zones and less stiffness will exhibit reduced neural density and type I to type III collagen ratio. Due to the high reoccurrence rate and career ending consequences of shoulder instability, it is vital to understand all the components that maintain shoulder stability, especially neural signaling that may be affected by changes in neural density . This study will aide in the development of specific treatment approaches for preventing or treating shoulder instability.

Last modified: Jul 22, 2016
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