Current Students

Linda D'Silva Pic

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. 

   
Stefanie Kennon-McGill Pic

Stefanie Kennon-McGill

Grad Student, Department of Otolaryngology

Project 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.
 
Anna Mattlage Pic

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.
 Jason-Flor Sisante picture

Jason-Flor Sisante
Grad Student, Department of Physical Therapy and Rehabilitation Science

Project Title: The effect of exercise on brain blood flow, cognitive performance, and neurovascular biomarkers following acute stroke

Research Mentor: Sandra Billinger
Co-Mentor: John Stanford

Stroke survivors exhibit altered blood flow and cerebral autoregulation, specifically on the ipsilateral side of the stroke.  Poor regulation of brain blood flow may impair delivery of oxygen and nutrients to the parenchema and could affect cognitive performance.  In non-stroke populations, previous research has shown that exercise improves blood flow and cognition, but not much is known about the effects of exercise on brain blood flow and cognition following acute stroke. Using transcranial Doppler ultrasound, cognitive batteries, and a submaximal exercise protocol, this project will investigate the effects of exercise during acute stroke recovery on brain blood flow, cognitive performance, and neurovascular biomarkers. This work may elucidate whether cerebral blood flow regulation and cognition improves as a result of exercise early after stroke.  We will also examine neurovascular markers that may be associated with changes in our outcome measures. This work has important implications for acute stroke rehabilitation and may help improve patient-centered outcomes.

Matt Stroh Picture

Matt Stroh
Grad Student, Neuroscience

Project Title: Understanding the role of iron homeostasis and mitochondrial function in a mouse model of neurodegenerative disease and diabetes

Research 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.

Last modified: Jan 30, 2014
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