Projects

16 Results
Fundraising Campaign
by Donors Cure

Funding for biomedical research is at an all-time low, and as a result, one of the greatest challenges to both the progress of research and the retention of young scientists is obtaining a continuous source of funding.

Travel Campaign
by Ariana Farrand

I will be presenting my research at the Society for Neuroscience (SfN) conference in San Diego this November. My research is centered around developing a protective treatment for Parkinson’s disease in rats that may slow disease progression, and studying how our treatment is creating its effects. Parkinson’s disease is the second most common neurodegenerative disorder with approximately 50,000 new cases being diagnosed in the United States each year. Existing treatments for Parkinson’s patients, while effective to treat symptoms, do not slow the underlying disease progression, eventually rendering additional symptomatic treatment ineffective.

SfN is an international meeting attended by leading experts in neuroscience that I would not otherwise have a chance to meet. Presenting my research at this meeting will provide an invaluable forum for discussion with these individuals. During the first day of the conference I will also attend a course on movement disorders, providing the opportunity to learn from and network with experts in my more focused field of Parkinson’s disease. Networking at SfN this year in particular will be vital. I am in my final year of study and will be building relationships to foster future collaborations and career advancement opportunities as I move forward this year.

Nervous System, Parkinson's disease
Funded!
Travel Campaign
by Stewart Cox

Empathy is the action of understanding and vicariously experiencing the thoughts, feelings, and emotions of another. Simply put, it’s the derivative of the cliched expression “put yourself in someone else’s shoes.”

Interestingly enough, the ability to understand another’s feelings is not exclusive to humans. It has been demonstrated that many animal species, including rats, exhibit certain forms of empathetic behaviors.

With the help of his lab members, PhD student Stewart Cox has developed a new model of studying empathy in rats, in hopes of better understanding empathy in humans. The team hopes that this new model will improve therapies for individuals suffering from cognitive disorders where empathy is affected, like substance abuse.

Stewart is traveling to the Society for Neuroscience to present his lab’s findings.

Addiction
Funded!
Travel Campaign
by Brandon Hughes

Brandon is studying the link between environmental triggers and relapse in addiction. The goal is to identify where and what in the brain causes withdrawal (which leads to relapse) after a trigger happens.

Brandon's team is currently working on mice to understand the regulatory mechanisms between the relation of the memory (trigger) and the exposure to the addiction (drug). This is the first time Brandon will attend the Society for Neuroscience where he hopes to network and collaborate on future projects.

Addiction
Funded!
Travel Campaign
by Daniel Lench

I am planning to present my research at the American Society of Neurorehabilitation (ASNR) in San Diego this November. ASNR is a unique opportunity to share my work with other scientists in the field of stroke recovery and get feedback. It is important to note that I am currently in my 4th year (entering my last year) as a PhD student. This conference will be critical in my ability to identify future post-doctoral career opportunities and build relationships with collaborators as I move towards becoming an independent investigator.

Stroke is the leading cause of physical disability in the United States and affects more than 795,000 Americans each year. My research focuses on understanding the brain reorganization that occurs in the motor network of these patients and how they relate to movement recovery. We've found that stroke disrupts the ability for the left and right motor network to communicate properly. Ultimately this research aims to understand what brain reorganization patterns contribute to successful rehabilitation outcomes.

Nervous System, Stroke
Funded!
Travel Campaign
by Ana-Clara Bobadilla

Dr. Bobadilla speaks about her journey to the Society of Neuroscience, where she found her post-doctorate job through networking and presenting there. This year, she heads back to the conference which takes place in San Diego and will once again be showcasing her work.

It was after presenting her work at the Society for Neuroscience conference in 2014 that she met Dr. Kalivas who asked her to start her first post-doctoral year at MUSC. Her study focuses on understanding the activity of the brain as it experiences a "trigger" that results in the relapse of drug addiction.

Addiction
Funded!
Research Project
by Rahul Desikan

Late-onset Alzheimer’s disease (AD), the most common form of dementia, places a large economic and financial burden on families and society and can be emotionally devastating to loved ones. While we know several things can affect AD, it is an incredibly complex disease, and there are likely other risk factors of AD that we still don’t understand.

Over the past two decades cardiovascular disease (CVD) is being increasingly recognized as an important risk factor of AD. In this project, we are interested in seeing if there are specific changes to genes that are risk factors for CVD and risk factors for Alzheimer’s disease. If we can find genetic risk factors that overlap between CVD and AD, we could target these genes to prevent or delay the onset of Alzheimer’s disease.

One way to identify the genetic risk factors for CVD that are also risk factors in AD is through large-scale genome-wide association studies (GWAS). In GWAS, human genomes – typically ones without a disease and ones with a disease – are compared to see if there are specific changes (or ‘genetic variants’) in the genomes of individuals with a specific disease.

In this project, we plan to take GWAS a step further by using the genomes of patients with CVD to find new genetic risk factors for AD. By using this approach, we intend to identify a subset of genetic variants that are risk factors for dyslipidemia, inflammation (two CVD traits that can be treated and prevented) and AD. As a second step, to understand the role of these risk factors in AD, we will then investigate the relationship between each of these genes and known pathobiological markers of AD.

1) Identify and validate genetic variants associated with AD and CVD traits. We plan to use GWAS to identify genetic variants that are common to traits of CVD (dyslipidemia and inflammation) and AD.

2) Determine the effect that these common genetic variants have on clinical and neuropathological measures of AD. We will determine the relationship between AD/CVD genetic risk variants and the presence of markers known to be elevated in AD.

Late-onset Alzheimer’s disease (AD), the most common form of dementia, effects an estimated 30 million people worldwide, a number that is expected to quadruple in the next 40 years. In the brain (or ‘neuropathologically’), AD is characterized by the presence of amyloid-beta plaques and tau-associated neurofibrillary tangles. Since there are no current disease-modifying therapies and there has been an increasing awareness that symptoms of AD develop over many years, there is a strong need to develop effective strategies to prevent AD. If we could even delay the onset of dementia by a modest 2 years, we could potentially lower the worldwide prevalence of AD by more than 22 million cases over the next 40 years.

Although previous studies have examined the association between AD and CVD traits, no study to date has fully identified the genetic and molecular basis of how dyslipidemia and inflammation influence AD. This project will provide us with a clearer understanding of how CVD and AD are related.

 Additionally, this study is the first step in research that is expected to lead to the development of novel strategies for preventing AD. Dyslipidemia and inflammation are effectively managed through current therapeutics; therefore, if we can identify an overlap between the genetic variants causing these CVD traits and AD, we could use drugs targeting dyslipidemia and inflammation to also treat, prevent, or delay AD. 

Alzheimer's Disease
Funded!
Research Project
by Shannon Risacher

Alzheimer's disease is a major public health crisis affecting millions of Americans. The current focus for treatment development is for treatments that are administered in the earliest stages of disease, before a clinical diagnosis of Alzheimer's disease. In addition, many research projects are investigating the causes of Alzheimer's disease and the course of how the disease progresses starting from the earliest stages of disease. In order to effectively target future treatments and to properly investigate the early stages of Alzheimer's disease, non-invasive and inexpensive measures to detect early biological changes associated with Alzheimer’s disease, even before cognitive symptoms develop, are needed. These markers would be useful for clinical research, diagnosis and screening, as well as for clinical trials of potential therapeutic treatments.

The goal of this project is to evaluate whether targeted markers of visual function could be used to detect biological changes associated with Alzheimer's disease in early stages. Many people forget that the retina is part of the central nervous system and has many biological and cellular properties that are similar to those seen in the brain. Therefore, we believe that measures of retinal structure and function may give us information about biological changes going on in the brain, including those that happen in the early stages of Alzheimer's disease, specifically the accumulation of the protein deposits thought to cause Alzheimer's disease (amyloid-beta plaques, tau neurofibrillary tangles).

Our project will evaluate individuals at risk for Alzheimer's disease with targeted visual tests of retinal function, specifically evaluating contrast sensitivity (ability to distinguish dark shades from light shades), and retinal structure (evaluating whether certain retinal layers show degeneration). These individuals will also undergo clinical and cognitive testing and neuroimaging scans to look at brain structure and function (MRI) and to determine whether these individuals show evidence of amyloid and tau deposition in their brains (PET). Our goal is to determine whether the visual measures predict the presence of amyloid and tau in the brain, as well as changes in brain structure and function, even in individuals who don't yet have cognitive decline.

If successful, we hope to establish these visual measures as useful screening tools to evaluate older adults for risk of having pathology associated with Alzheimer's disease. Ultimately, we could see these tests being done on a regular basis at an ophthalmologist office or even in a primary care setting as a screening test for Alzheimer's disease pathology. Then, in the absence of a known reason for an abnormality on the test (i.e., diagnosed eye disease), if an individual does poorly on the contrast sensitivity test and/or shows degeneration of their retina, they could then be sent for more extensive testing with a Neurologist, including perhaps MRIs and amyloid and tau PET scans (or other future tests). We hope that one day these tests could be used in clinical practice to assist with screening for Alzheimer's disease and in clinical trials of new therapeutics to screen individuals for those most at risk for having Alzheimer's related pathology. Ultimately, once an effective drug is developed, we envision using these tools to screen individuals for disease and suggest additional testing to determine whether they should be given the treatment.

Alzheimer's Disease
Funded!
Research Project
by Rachel Buckley

Identifying and monitoring memory changes in individuals that are at risk of Alzheimer's disease (AD) dementia necessitates serial cognitive testing in a memory clinic. As clinical trials move to test novel therapeutics much earlier in the disease, two factors are critical for their success: 1) very large sample size to detect subtle memory changes, and 2) multiple testing centers across cities and countries, which requires highly-standardized tests. Annual and in-clinic cognitive assessments are conventionally used to monitor memory changes in studies, as this is considered a well-validated and accurate method of gauging cognitive performance. This method, however, is extremely time-consuming, labor-intensive, and difficult to standardize across centers and countries. It also reduces results in the recruitment of only those individuals who are willing to travel in to a memory clinic and do hours' worth of testing; as such, studies are likely to recruit participants who are highly motivated, well educated, physically healthy, and/or low in racial diversity, which can skew estimates of cognitive change. This is particularly problematic for clinical trials, as they normally gauge the efficacy of a drug based off of cognitive change estimates gleaned from these biased observational studies. Inaccurately estimated cognitive trajectories can have major implications for the success of these trials, as the success and failure of drug trials are often predicated on a cognitive endpoint. In addition, the most comment method for gauging cognitive change is via annual assessments, which introduce issues of signal-to-noise and regression to the mean, such that random error may also obscure the rates of change.

Recent work in computerized testing has reintroduced the possibility of more frequent assessments. Further, in-clinic studies of high-frequency testing have shown that this method is reliable and more accurate than annual assessment. What is unclear, however, is whether high-frequency testing can be translated to the internet. In this situation, individuals would regularly self-administer their own cognitive tests for researchers to monitor remotely.

The objective of this proposal is to assess the feasibility and reliability of online, high-frequency cognitive testing in a large group of clinically-normal adults. This proposed study will capture "burst design" monthly memory performance over a period of 12 months in a group of 400 participants (40-65 years; 200 APOE 4 carriers/200 non-carriers), and, in a separate group of 400 participants, annually (at baseline and after 12 months). All participants will be recruited from the Australian Healthy Brain Project (www.healthybrainproject.org.au), a large (n=5000) online study of brain health in clinically healthy Australian middle-aged adults between 40-65 years. By examining high-frequency, online cognitive testing over the span of a year, this study will determine the applicability of this method to better track cognitive trajectories in comparison with annual cognitive testing. Further, this study will determine whether high-frequency cognitive assessments can detect the well-characterized cognitive decline trajectories seen in those with genetic risk for Alzheimer's disease sooner than shown in annual cognitive assessments.

In an effort to improve measurement of cognitive change in middle-aged adults, the proposed study provides an unprecedented opportunity to rethink the way cognitive decline trajectories are currently measured and estimated. Outcomes from this study will aid in the development of new approaches to measuring the very earliest cognitive changes in those at risk for Alzheimer's disease. In addition, this has consequences for the ability of observational studies to inform clinical trials on likely cognitive trajectories in populations of interest and has the potential to lead to more accurate estimations of treatment effects.

Alzheimer's Disease
Funded!
Research Project
by Kristine Wilckens

Late-life changes in sleep are thought to contribute to cognitive dysfunction and progression of Alzheimer’s Disease. Sleep disruption impairs multiple aspects of cognition. This connection may occur through slow-wave sleep which characterizes the deepest, most restorative stage of sleep. Slow-wave sleep is commonly associated with memory in both young and older adults. Intriguingly, during slow-wave sleep, beta amyloid, a precursor for Alzheimer's disease, is cleared from the fluid surrounding the brain, suggesting a direct link between slow-wave sleep and prevention of neurodegeneration. Accordingly, treatments that enhance slow-wave sleep in older adults are thought to be promising for preventing and delaying neurodegeneration. Slow-wave sleep can be enhanced through wake activities in a use-dependent pattern. For instance, brain stimulation during wakefulness can lead to a robust increase in slow-waves during subsequent sleep. Brain stimulation outside the sleep field has been shown to benefit memory in patients with depression and mild cognitive impairment (MCI). Slow-wave sleep regulates brain plasticity and reorganizes neural connections to enhance relevant memories and the function of brain networks involved in memory. Thus, slow-wave sleep may drive memory enhancement through brain stimulation. This pilot study will compare increases in slow-wave sleep and memory performance before and after brain stimulation over the dorsolateral prefrontal cortex in older adults with MCI. It will assess whether brain stimulation increases slow-wave sleep and memory in MCI, and explore whether slow-wave sleep increases are associated with memory improvements.

Alzheimer's Disease
Funded!
Research Project
by Cristina Lopez

Approximately 20 million adults in the U.S. with diabetes are of low-income and minority populations. This population has an increased vulnerability to diabetes due living in high-stress environments, victimization from violent crimes, family history of domestic violence, personal histories of child physical and/or sexual abuse, and witnessing repetitive community violence. Common health disparities are often overlooked and access to appropriate medical care can be limited. Patient education for diabetes does not address how these previous traumatic experiences affect patients' ability to be compliant with their diabetes treatment plan.

While the effects of mental trauma on health disparities related to Type 2 Diabetes have focused largely on major depression, there is growing evidence that posttraumatic stress disorder (PTSD) is also associated with chronic disease and with poorer health outcomes. A potential contributing factor to the detrimental effects of PTSD and self-management for diabetes is an individual’s difficulty with regulating emotions and stress. Customized modifications of diabetes self-management could help increase patient engagement in both PTSD treatment and compliance with their own diabetes treatment plan. This study will be the first to examine effects of mental trauma as a contributor to the link between trauma exposure and diabetes self-care. The sample population consists of adults that are predominantly from ethnic minority groups (Latino and African American) and all are un-insured, lower socioeconomic families.

In this study, we will be able to look at electronic medical records of patients at two community clinics (Harvest Free Community Clinic and East Cooper Community Outreach (ECCO)) that are well-respected and trusted by this underserved and high needs population.

Individuals will be asked if they would be interested in participating in our survey study, which would involve completion of self report survey to gather information about each patient's emotion regulation, interpersonal violence and abuse history, PTSD symptoms, depression, daily diabetes self management activities, and positive/negative mood. Staff will also gather information from their electronic medical record (EMR) about their HbA1C, medications, other chronic conditions, BMI, and glucose levels. Most importantly, 10 of the participants will be asked to join in a group feedback session with the researchers to share from their perspective what their barriers are to managing their diabetes so that this information can be incorporated into appropriate health interventions. 

While some studies may link the connection between PTSD and diabetes with biological changes in the stress regulating systems of the body (e.g.,  dysregulation of stress reacting hormones like cortisol), this study will determine whether the socio-emotional aspects related to health decision making behaviors may also lead to the development of type 2 diabetes and continue to contribute to poor management of diabetes. 

Emotion regulation refers to how each individual handles intense emotions and/or stress (e.g., overeating, becoming more sedentary, impulsive poor choices, forgetfulness). By examining the role of emotion regulation in diabetes management, we can tailor diabetes self management to increase patient engagement in compliance with diabetes treatment plans as well as patient engagement in treatment for PTSD symptoms.

In addition to recruiting enough patients (100) to conduct analyses that are reliable and accurate, we are also relying on the input of patients from this victimized population, who can tell us first-hand what obstacles may be affecting their diabetes self management and can let us know what strategies will be most accepted in their community and how best to share this information with the community in need.

Results from the proposed study will provide pilot data for the NINR R21 application  to develop proper modifications to PTSD treatment and/or customized diabetes self-care activities to prevent patient drop-out and/or noncompliance. 

Diabetes
Funded!
Travel Campaign
by Krishna Bharani

The Fourth Annual Symposium for Advocates of Women in Science and Medicine will be held Saturday, March 25th, 2017 at the University of Virginia. There will also be a multi-professional networking dinner following the symposium. This will be a day focused on career advancement and advocacy for women in science and medicine!


This year's symposium will feature Dr. Vivian Pinn as keynote speaker, who will share her pathway through medical training as well as her work on advocating for women in science and medicine. We will also have Kimberley Barker speak on managing online presence as a medical and/or research professional. In addition, the day will include a poster session, networking workshops, and focused panels on topics including career development, work-life balance, and inter-professional collaboration.

We have a group medical and graduate students who will drive up from Charleston, SC to Charlottesville, VA to attend the Fourth Annual Symposium for Advocates of Women in Science and Medicine. 

We hope to raise some money to help fund our lodging for two nights at the conference. 

The goal of this meeting is to educate members about inequalities women in research and medicine face and generating educational and networking experiences for students to help overcome these obstacles. This symposium importantly brings together advocates (male and/or female) for women in science and medicine (from across many disciplines) to facilitate discussion of challenges, goals, tools, and opportunities women face in science and medicine. By including participants from across medical, graduate, and nursing education we can have in depth conversations and facilitate connections across these disciplines (adapted from http://uvaaffirm.wixsite.com/southeastsymposium).

Advocates for Women in Science & Medicine
Funded!
Research Project
by Dana Szeles

This project will examine the role of cholesterol-lowering medications, i.e. statin therapies on the brain. The goal of statin therapy is to prevent the occurrence of heart attacks and stroke by lowering one’s cholesterol, thereby regulating plaque build-up and vascular events. However, cholesterol is also a vital building block for myelin, which provides support for the brain and its connections. Since cholesterol is a vital component of myelin, and myelin is critical for cognitive function, changes in cholesterol levels by statins may also impact cognition.

 In 2012 the FDA issued a warning that changes in memory and thinking were a known side effect of statins. As most research completed to date has been aimed at identifying risk reduction for vascular events, previous studies have not examined the direct impact of statins on brain function. The mechanism for this relationship therefore remains unclear. Furthermore, it remains controversial whether women derive the same risk-reducing benefits as men and they often experience a greater number of side effects. Despite this, women have historically not been as involved in clinical trials. We seek to address these gaps in the literature.

This study uses quantitative high field (3 Tesla) Magnetic Resonance Imaging (MRI) and cognitive testing to evaluate the brain’s microstructure and function. We plan to perform a longitudinal study, evaluating patients’ brains before initiating treatment and after 12 weeks of statin use in 20 women ages 45-85. The same procedures will be performed on 10 age-matched controls who are not prescribed or taking statins.

At the completion of this project, we aim to successfully quantify the effects of 12 weeks of statin therapy on the microstructure and function of the brain. In doing so, we hope to elucidate the possible effects of statin use on brain function, and offer a potential mechanism for observations of even subtle cognitive dysfunction in otherwise neurologically healthy adults.

In response to the increasing number of heart-related deaths and rise in heart disease in the U.S. statin drugs were first introduced in 1987 to reduce cholesterol levels in the body. According to the National Center for Health Statistics, statin use increased from 20 to 28% over the period of 2003-2012, reflecting a tremendous expansion in how these drugs are now prescribed. Importantly, in 2012 the FDA issued new warning label changes that identify memory loss and confusion as significant side effects, though this has seemingly not impacted prescription rates. By quantifying the microstructural and cognitive changes that accompany statin use, this study aims to generate objective evidence on the effects of stain use on the brain. Critically, this may catalyze future investigations on the specific indications and conditions required to justify statin use and support the identification of individuals particularly vulnerable to its effects.

Hypercholesterolemia
Funded!
Travel Campaign
by Tanja Kellermann

My study is the first to use a novel brain imaging technique that allows us to examine the structural details of the brains of children with epilepsy. We can then connect these structural details to symptoms of depression found in these children. In more specific detail, my study links neuropsychological measurements with structural brain imaging to evaluate whether depressive symptom are associated with specific volume changes in the brains of children with epilepsy. Twenty-five children with epilepsy were evaluated for depressive symptoms and were imaged with magnetic resonance imaging (MRI). The study found that in specific brain regions there was an increase in gray matter volume that was associated with a higher overall depressive symptom severity. Further, specific groups of depressive symptoms are associated with gray matter changes in the same brain regions. These findings provide evidence for progressive reorganization of brain networks, supporting the presence of diverse patterns or clusters of depressive symptoms in children with epilepsy. Knowledge that specific brain regions are involved in depressive symptoms may help tailor and improve treatments and subsequent outcomes over the course of epilepsy and quality of life. 

My aim is to improve our understanding of the neurobiological changes that occur in children with epilepsy and the associated cognitive and behavioral health comorbidities, and to identify biomarkers that may assist in predicting the effect of (non-)surgical treatments. My research combines clinical and neuroimaging techniques to examine behavioral health functioning in children and adolescents with epilepsy. Understanding how and when comorbidities, such as depression, anxiety, learning disorders and ADHD occur with epilepsy could lead to improvements in the way we identify and treat both epilepsy and its comorbidities.

My research was accepted for presentation as a poster at the largest, most well respected, and innovative scientific meeting in the field of epilepsy - the American Epilepsy Society (AES). Why is it important for me to present this data? Perhaps, one of the most important benefits is the ability to advocate for children with epilepsy by presenting my findings to other epilepsy researchers and clinicians, but also to increase public awareness of this innovative research in my field. Because my research provides a link between interdisciplinary fields, it is imperative that I interact with other excellent researchers from different fields and exchange ideas, as well as receive productive feedback about my work. Attending the AES meeting in Houston in December and presenting my findings will give me the opportunity to discuss my research and learn valuable information from people working with similar techniques and populations.

Epilepsy is one of the most common neurological disorders during childhood and adolescence. More than 450,000 children and adolescents in the United States currently live with epilepsy. Odds of depression in this population are threefold compared to healthy children, but also higher than in kids with other neurological disorders (e.g., migraine), suggesting that neuropathophysiological and/or psychosocial factors (e.g., uncertainty associated with unpredictability of seizures, social isolation, independence with self-management, and driving restrictions), specific to epilepsy may provide more “insult” for children with epilepsy.

Given the complexities of depression in children, it is important to examine specific symptoms of depression in children with epilepsy. To date, no study has investigated structural brain changes in relation to specific clusters of depressive symptoms. The current study is the first to use a specific brain imaging technique called voxel-based morphometry (VBM), which allows the examination of differences in brain anatomy, to relate structural brain changes in children with epilepsy to different clusters of depressive symptoms. The proposed project is significant for the following reason: it will potentially identify a biomarker for epilepsy comorbidities and inform further needed research regarding brain networks, epilepsy comorbidities, and neuroimaging in children with epilepsy. Understanding how different depressive clusters relate to specific brain regions could inform treatment methods and decrease the severity of epilepsy comorbidities. 

Epilepsy
Funded!
Research Project
by Palmer Freshley

I will be conducting research alongside Dr. Ablonczy to scan for physical changes in retinas in response to glycation products and B-amyloid substances. Diabetic macular edema (DME) is the accumulation of fluid within the extracellular spaces of the neuroretina. DME is a principal cause of vision loss in diabates, thereby carrying enormous social and economic burdens. Early studies focused on leaky retinal blood vessels as the principal source of the edematous fluid. However, more recent data suggest that impaired fluid transport from the neuroretina by the retinal pigment epithelium (RPE) plays a critical role in the accumulation of fluid. Our long-term objective is to understand how endogenous and environmental factors impact the ability of the RPE to maintain extracellular fluid balance in the retina and prevent edema.

The pattern recognizing receptor for advanced glycation end-products (RAGE) belongs to the immunoglobulin super-family. The activation of RAGE has been shown to contribute to a variety of conditions: Alzheimer disease, cardiovascular and microvascular disorders, tumor angiogenesis, and atherosclerosis. One of the high-affinity ligands of RAGE is amyloid-42. During aging or metabolic stress, amyloid-42 is increased in ocular humors leading to the activation of RAGE in the RPE. New data from our laboratory provides evidence that RPE barrier function is compromised by amyloid-42 and that ihibition of histone acetylation reverses this response. The goal of this project is to understand the role of amyloid-42 in the breakdown of RPE fluid transport, so that we can design medications to treat diabetic macular edema.

Current treatments of DME are risky and invasive. Therefore, new approaches are required for efficient and safe pharmacological interventions to stop or reverse the condition.

Diabetic retinopathy
Funded!
Travel Campaign
by Emilie McKinnon

Aphasia, or language impairment permanently affects one third of patients surviving a stroke in the left hemisphere.  Speech therapy can be effective to improve communication for some patients, but unfortunately, not everyone responds well to treatment and to date little is known about what drives rehabilitation success.  A popular hypothesis suggests that recovery-related neuroplasticity is associated with the strengthening or the re-establishment of structural connections between key related brain regions. In this study, we aimed to test this hypothesis by assessing the relationship between therapy-related improvements in naming errors and microstructural white matter fiber properties, using innovative assessments of mean kurtosis (MK), which is a novel and sensitive metric of microstructural complexity, measured longitudinally along white matter pathways associated with the dorsal and ventral stream for language processing.  Our results suggest that with therapy the center of the ILF becomes increasingly complex if less semantic errors are made. Contrarily, the SLF displays a more complex microstructure if more phonetic errors are made, possibly a reflection of a therapy related increase in speech production.  These results likely fit the dual stream model for language, as changes in the dorsal pathway (SLF) correlated with changes in articulation and changes in semantics reflected as microstructural changes in the ventral stream (ILF). 

I would love to present this abstract at the annual meeting of the society for the neurobiology of language. Upon finishing my first year as a PhD student, I am most eager to learn about the latest discoveries in the field and how I can integrate these in my own work. I still have a lot to learn about neuroscience, especially how it applies to language. Hence, I believe that attending SNL will be very fruitful for my professional advancement. During the last semester, I attended an 8 semester hour course on the fundamentals of neuroscience, providing me with the basis to understand the work presented at the conference. I am excited to start studying the neurobiology of language, and I believe that attending this meeting will significantly impact my work. The opportunity to share my work and meet with leaders in the field will be an excellent way to establish myself.

Cerebrovascular accidents are the leading cause of disability in the United States. Aphasia, a deficiency in language processing, is common consequence of a dominant hemisphere stroke and often associated with significantly reduced quality of life. The symptoms of aphasia can vary across different
subjects, including different degrees of difficulties in producing and understanding language. Treating patients with aphasia is complex and consists in multiple and intensive sessions of speech therapy. Unfortunately, not every patient responds well to therapy and to date little is known about what guides post-ischemic tissue remodeling, neuroplasticity, stroke and aphasia recovery. If we were able to better understand the mechanisms associated with recovery from cerebrovascular injury, this information could be used to improve patient counseling, guide treatments and improve therapy approaches.
A popular hypothesis suggests that recovery-related neuroplasticity is associated with the strengthening or the re-establishment of structural connections between key related brain regions. We propose to use neuroimaging to assess the neuroplasticity of stroke recovery by studying structural brain changes induced by speech therapy, as well as by evaluating how spontaneous recovery and speech therapy are associated with the reorganization of neuronal networks. The significance of this project is twofold. First, the investigation of structural changes could provide new insights related to the neurobiological mechanisms associated with stroke recovery. Second, by investigating personalized patterns of tissue integrity, this research may lead to the development of markers for recovery potential after a cerebrovascular incident.

Aphasia
Funded!
Research Project
by Christine Dixon Thiesing

The Gotbeters, a local Charleston family, adopted their daughter, Molly, from China when she was three years old. Unlike most toddlers, Molly has spina bifida, a birth defect where, early in embryonic development, a portion of the neural tube doesn’t close properly near the base of the spine. Since adopting Molly, the family has been working with doctors to get her treatment, which has required many doctor’s appointments.

As anyone who visits the doctor knows, one of the most common ways to quickly test for a myriad of conditions is through a urine sample, and with Molly’s condition, this was something that had to be done often.. Have you ever tried to get a urine sample from a wriggling, impatient three-year-old? It’s a feat. If getting a ‘clean’ sample isn’t possible, the next step is to use a catheter, which is even more traumatic – for anyone at any age. 

Spurred on by an advertisement by the MUSC Foundation for Research Development (FRD), the university’s tech transfer office, the family submitted an idea they had come up with for a urine collection device that would make their lives – and the lives of other parents trying to take urine samples from children – easier. Not only is this device helpful for obtaining hygienic samples from children, it is useful for anyone who has a difficult time voiding while holding a cup, such as the elderly and hospital patients. 

The device is simple: it is a disposable, urine collection system that has a plastic liner that release-ably mounts to a toilet bowl, rim or seat, and contains a basin in the center for the urine. The basin has a stopped port that can drain the urine into any specimen container. It fits on a variety of toilet sizes, ranging from a toddler potty to a full-sized toilet seat. Because it is hands-free, it allows for a more hygienic collection and makes the process simpler, particularly when holding a cup is challenging or impossible.

Thankfully Molly had surgery last year to  fix the majority of the effects, and she is a happy four-year-old, but there is a very large population that are still in need of an easy and hygienic way to collect a urine sample for their health.

A provisional patent application has been filed for this device, and we currently need to develop a working prototype. These funds will be used to support building the prototype, which we will use as a working model to help license the technology, and ultimately have this product go to market.

 This device works for any and all applications that may require urine collection and for all populations.

Urinalysis is performed as a part of most routine medical examinations, including pregnancy checkups and drug screening, and is necessary for diagnosing and monitoring conditions like urinary tract infections, kidney and bladder disease, and back or abdominal pain. The ‘clean catch’ method is typically used to collect urine samples to avoid contamination, but this is difficult for most to complete hygienically. Additionally, if a patient needs assistance, the process can be unsanitary and embarrassing, and if it is too difficult, the doctor may end up having to use a catheter, which is uncomfortable and even painful. 

While there are other urine collection systems, all current devices have limitations such as not being disposable or not being configured to fit specific specimen containers. Additionally, they don’t fit a range a toilet sizes. 

Devices
Funded!