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Doctoral Program in Neuroscience
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Admission Requirements

For the Program

The Roskamp Institute offers a doctoral degree in Neuroscience.

Prospective candidates for admission for the Ph.D program must have:

  • For UK students: a Bachelor’s degree of class 2.1 or higher in a biological sciences field.
  • For US students: a Master’s degree in a biological sciences field or a Bachelor’s degree plus either one year of post-graduate full-time laboratory research at the Roskamp Institute or two years of post-graduate full-time laboratory research with another institution and demonstrated productivity.
  • For students from other countries: equivalency to either UK or US student requirements as stated above.

Selection and Admissions Policy

We utilize a three-part selection process.



Step 1: The Program Administrator reviews applications for completeness and eligibility.

Step 2: Eligible applications move to the screening committee which reviews the applications and identifies candidates for interview.

Step 3: Applicants are interviewed in-person or by video-conference by the Roskamp Admissions Committee (which consists of all supervisors and potential supervisors). This committee evaluates the candidates based on eligibility, suitability for the program and for the available projects, and overall qualifications (intellect, motivation, aptitude, existing skills, and personality) as a PhD candidate.

Admission will be based on an evaluation by a Roskamp Institute committee. The Admission process will weigh many factors including the applicant’s scholastic record, prior performance in laboratory research, letters of recommendation, statement of purpose, and ultimately personal interviews. Successful candidates will be offered a position.

Example PhD Projects

Therapeutic target identification through analysis of microglial driven traumatic brain injury pathogenic mechanisms.

Traumatic brain injury (TBI) is a major cause of mortality and morbidity among both military personnel and the civilian population and is the leading cause of death and disability in the under-45 age group in industrialized countries. Among the soldiers who survive conflicts in Iraq and Afghanistan, TBI accounts for a larger proportion of their casualties than in any other war in recent US history. Furthermore, among patients evaluated at the Walter Reed Hospital, closed head injuries significantly outnumber other penetrating injuries, and although blast injuries have gained much attention in recent years, 84% of TBIs occur in a non-deployed setting involving vehicle crashes, falls, sports and military training activities (Defense and Veterans Brain Injury Center statistics).

The Centers for Disease Control and Prevention estimates that 5.3 million Americans are living with disabilities resulting from TBI. In particular repetitive mild TBI is now recognized to be a major health concern for both civilian and military populations. These repetitive injuries may result in dementia-like symptoms where the patient may experience memory loss, aggression, confusion and depression. For many years TBI has been known to be a risk factor for Alzheimer’s Disease (AD) and other neurodegenerative conditions, but the precise nature of how TBI leads to or precipitates AD is not understood. Current treatments for TBI focus on the primary consequences of the injury, such as brain swelling, as the chronic biological consequences of TBI are still mostly unknown. There are very few current clinical trials in the US or even worldwide which are specifically addressing mTBI, and typically the drugs under investigation were developed for other conditions and have shown very little success thus far, presumably due to the lack of knowledge of the molecular mechanisms which constitute the brains’ secondary response to TBI. These numerous and complex mechanisms may persist for months and even years after the event, and naturally are significant contributors to the patient’s outcome.

The goal of this proposal is to validate these lipid changes as targets for TBI therapeutics. This work will, in two years, provide critical information on potential therapeutic targets to mitigate the chronic neurodegenerative consequences of TBI, and will provide preliminary data on treatments which may be effective in that regard. This will provide a laboratory based platform for future studies to further evaluate these targets and compounds, with experiments designed to translate the basic science into clinical practice- namely studies of how different doses or administration paradigms influence the outcome after TBI; when the optimum treatment window occurs; how the compounds are distributed and metabolized in the body. This project will thus be of considerable significance in identifying novel approaches and effective treatments for TBI and will contribute to the much needed increase in flow of viable, TBI focused treatments into human clinical trials.

Delineating the contribution of tau astrogliopathy to the neurodegenerative sequelae of repetitive mTBI.

Traumatic Brain Injury (TBI), in particular repetitive mild TBI (r-mTBI), is a major cause of disability in military and civilian populations, and for many years has been known to be an epigenetic risk factor for Alzheimer’s Disease (AD) and related dementia (ADRD).

However, the precise nature of how TBI leads to or precipitates ADRD pathogenesis is not understood. To address this problem, we have, in a previous contract, used our well-characterized 5-hit mouse model of r-mTBI to generate molecular profiles of TBI pathogenesis at a range of timepoints post-injury, which we then compared to molecular profiles of AD pathogenesis in AD mouse models as they aged.  This enabled us to identify molecules and pathways common to both AD and TBI, and to correlate these with longitudinal changes in cognition and in the neuropathological landscape. Our preliminary data suggest a distinct TBI related neurodegeneration which shares features with AD and ADRD features which develop with age. R-mTBI in young and aged models also results in different pathogenic consequences.

Neuroglia pathobiology appears to be a critical driving force in these models, particularly with astrocytic and microglial responses showing differential outcomes in the young and aged brain. Treatment paradigms targeting neuroinflammation in our TBI model have demonstrated proof of concept for the significance of neuroglial cells by ameliorating both neuropathological and behavioral changes, but more sophisticated targeting is clearly needed to tackle the specific responses which drive TBI pathobiology.  In an ongoing award, we have begun exploring the dynamic changes in reactive and dystrophic microglia phenotypes in TBI/ADRD pathogenesis using a novel single cell genomic approach, which we now plan to complement by conducting a comprehensive analysis of astroglia pathobiology across neuropathological stages of TBI and ADRD cases.

Understanding TBI neurodegeneration, and triggers that encourage the pathogenic sequelae of TBI to follow paths toward ADRD, will be critical to the identification of effective therapeutic approaches. This project will interrogate the role of astrocytes in the neurodegenerative sequelae of TBI, with the goal of identifying novel targets/techniques with which to manipulate astrocyte functions in vivo as a therapeutic strategy.

Submit Your

Application

Applicants for the program will be required to complete the following application form and submit to the Roskamp Institute Program Administrator who will screen for eligibility. Eligible applications will be reviewed by the Roskamp Institute Research Degrees Coordinator and by the Roskamp Institute Admissions Committee and competitive applications will be selected for interview in person or by tele/video conference.

For more information regarding this program, please contact [email protected]

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Location: 2040 Whitfield Ave., Sarasota, FL 34243

Telephone: (941) 752-2949

Email: [email protected]

Office Hours: M-F: 9am - 5pm

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