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Monday Sessions

Anniversary Lecture 01 

John Povlishock, PhD; Virginia Commonwealth University

Description

This is the 35th Annual National Neurotrauma Symposium. In celebration of 35 years of exchange of expertise and collaboration, the four founders of the National Neurotrauma Society will each give an anniversary lecture which highlights the past, present, and future of an enduring topic in neurotrauma.

Educational Objectives

  1. Identify the role of reactive oxygen species in the pathology of neurotrauma
  2. Understand evolving concepts of secondary injury and the therapeutic window
  3. Understand how neurotrauma research has advanced over the last decades
PL01:Neurotrauma-Induced Autoimmunity 

Chairs: Kevin Wang, PhD; University of Florida & Amy Wagner, MD; University of Pittsburgh

  1. Autoimmunity Response Following TBI: Is It Detrimental or Beneficial? - Kevin Wang, PhD; University of Florida
  2. Post-TBI hypopituitarism and anti-pituitary and anti-hypothalamus antibodies - Fahrettin Keleştemur, MD; Erciyes University  
  3. Post-TBI neuroendocrine dysfunction and its relation with autoimmunity - Amy Wagner, MD; University of Pittsburgh
  4. NMDA and Glutamate Receptor Peptides and Autoantibodies in TBI and Ischemic Brain Injuries - Svetlana Dambinova, PhD; DeKalb Medical Center

Description

During the transition from acute to chronic stages of recovery after both SCI and TBI, there is an evolving state of immunologic responses that could influences individual patient’s outcome. Recent human and animal model studies have now show that neurotrauma-induced autoimmunity response is an emerging form of post-neurotrauma immunologic responses. In a rat model of traumatic SCI, Dr. Popovich’s team has shown that B cells can produce pathogenic antibodies and impair recovery after SCI in mice (Ankeny et al. 2009). Similarly, human TBI blood containing autoantibodies against glia antigens such as MBP and S100B were reported. Dr. Wang’s laboratory also found an immunodominant autoantibody response to astroglial protein GFAP and its breakdown products in a subset of TBI patients (Zhang et al. 2014, Wang et al. 2016). It was postulated that autoantibody specifically targeting a major brain protein such as GFAP might trigger a persistent autoimmune attack of the CNS, thus negatively affecting TBI patient long-term outcome. Key neuroreceotprs also can be targets for autoantibodies - Dr. Dambinova and colleagues reported the release of NMDA-receptor and glutamate receptor peptides and autoantibodies against them following TBI or cerebral ischemia (Weissman et al., 2012). Lastly, Tanriverdi et al. showed the presence of anti-pituitary and anti-hypothalamic antibodies in patient serum 3 years after head trauma (Tanriverdi eta l., 2010) . It was proposed that such APA and AHA might be linked to post-TBI hypopituitarism development. Yet, others have argued that autoimmunity might be a protective physiological response to CNS trauma (Yoles et al. 2001).

Educational Objectives

  1. Learn about the state of the art knowledge on the field of autoimmunity response following both TBI and SCI in humans.
  2. Examine different views regarding the beneficial versus detrimental effects of autoimmunity in neurotrauma patients.
  3. Understand the methods employed in animal studies to model neurotrauma-induced autoimmunity.
  4. Describe the general methodologies used to quantify and characterize the autoantibodies to CNS antigens.
Data Blitz A: Mini Presentations 

Chairs: Gene Gurkoff, PhD; UC Davis & Ramesh Raghupathi, PhD; Drexel University

Description

The goal of this session is for participants to provide a 2 minute oral presentation as a “preview” of the key components of their poster presentation. Selected posters presenters will be invited to give an oral slide presentation which emphasizes the most important and innovative aspects of their research that will be presented subsequently in the poster sessions. The time limit for each presentation (2 minute maximum) will be strictly moderated with the expectation that each presenter will have no more than 2 slides. The format is an energetic and engaging introduction to the poster sessions.

Educational Objectives

  1. Learn about the state of the art knowledge on the field of autoimmunity response following both TBI and SCI in humans.
  2. Examine different views regarding the beneficial versus detrimental effects of autoimmunity in neurotrauma patients.
  3. Understand the methods employed in animal studies to model neurotrauma-induced autoimmunity.
  4. Describe the general methodologies used to quantify and characterize the autoantibodies to CNS antigens.
Poster Sessions 1 & 2: Group A 

Description

Poster Presentations and Trainee Poster Competition.  

Odd poster numbers present in the AM session; Even poster numbers present in the PM session.

Educational Objectives

  1. Understand the diversity of preclinical models for studying brain and spinal cord injury.
  2. Learn about the ways in which preclinical neurotrauma research is translated into clinical practice.
  3. Learn about current clinical trials in brain and spinal cord injury.
WiNTR Lunch Session: The Lab Notebook Evolution 

Moderator: Mayumi Prins, PhD; UCLA

Open to all registered delegates regardless of gender. Cost: $20 includes lunch.  RSVP: June 30 - Ticket required

Description

As much of our world has moved into digital data management, many laboratories have continued to use traditional modalities for collecting, recording and sharing data. The objective of this session is to introduce people to what online programs are out there and discuss pros and cons of them and ideally establish what would be the “ideal” approach to moving lab notebooks into the digital age. Vendors will be present to share their current programs so attendees can get exposure to them.

Educational Objectives

  1. Identify resources for digital storage and organization of laboratory records
  2. Evaluate tools for laboratory project management
  3. Discuss what elements are needed in a successful digital laboratory data and records management strategy
PL02: Pain After SCI: Plasticity, Activity & Treatment 

Sponsored by Craig Neilsen  Chairs: David Magnuson, PhD; University of Louisville & Claire Hulsebosch, PhD; UTMB 

  1. Pain and Locomotor Circuitry: Competitors for Attention - Catherine Mercier, PhD; Laval University, Quebec 
  2. Plasticity and Neuropathic Pain After SCI - John Kramer, PhD; iCORD
  3. Central and Peripheral Mechanisms of Hyperalgesia and Chronic Pain - Kathleen Sluka, PhD: University of Iowa

Description

Somatic pain and neuropathic pain are major problems after SCI and interfere, directly and indirectly, with recovery, locomotor activity and daily living. Our basic understanding of how and why pain develops after SCI is growing, but is still lacking. There appears to be a relationship between pain, activity and locomotor circuitry that is still poorly understood and translational studies are sorely needed. The three speakers suggested would cover the range from pain and locomotion in the absence of SCI, plasticity after SCI and finally neuropathic pain and clinical approaches.

Educational Objectives

  1. Describe how joint and muscle pain influences activity and locomotor circuitry.
  2. Define neuropathic pain, how it differs from other kinds of pain and why is it so difficult to treat
  3. Report what plasticity occurs after SCI that leads to neuropathic pain and if activity can modulate that plasticity
S01: Novel Aproaches to Target Mitochondrial Dysfunction Following CNS Injury: From Biomarker to Replacing the Damaged Powerhouse 

Chairs: Patrick Sullivan, PhD; University of Kentucky & Courtney Robertson, MD; Johns Hopkins School of Medicine

  1. Assessing CNS Mitochondria Damage Using Serum Biomarkers - Todd Kilbaugh, MD; Children's Hospital of Philadelphia
  2. Swapping The Powerhouse Of The Cell Out Following SCI; Intraspinal Mitochondrial Transplants In SCI - Alexander Rabchevsky; PhD; University of Kentucky 
  3. Transfer Of Mitochondria From Astrocytes To Neurons After Stroke - Kazuhide Hayakawa, PhD; Massachusetts General Hospital 
  4. Permeability Transition, Synaptic Plasticity and Neurodegeneration - Elizabeth Jonas, MD; Yale School of Medicine 

Description

Mitochondria and mitochondrial dysfunction seem to be pivotal players in determining neuronal cell survival or death following CNS injuries. Acute loss of mitochondrial function following injury can result in bioenergetics crisis that leads directly to necrotic cell death. Alternatively, sustained mitochondrial dysfunction can result in release of mitochondrial proteins that initiate apoptotic cell death pathways. Taken together, this would place mitochondria in a position to act as a central “death switch“ of the cell. As such, targeting mitochondrial dysfunction following injury has proven to yield promising results in various animal models and, more recently, in limited human clinical trials. This session will examine the latest, “state of the art“ approaches to use mitochondria as a novel biomarker and/or as a pharmacological target of CNS injury, as well as the latest findings regarding protective mitochondrial transfer between astrocytes and neurons following stroke and intraspinal mitochondrial transplantation following SCI.

Educational Objectives

  1. State the basic role of mitochondria in cells of the CNS.
  2. Define the neuropathological changes that occur following CNS injury due to mitochondrial dysfunction and/or loss.
  3. Identify the pivotal role of mitochondria in CNS injury and the potential of using mitochondrial integrity as a biomarker.
  4. Define novel mitochondrial-targeted therapeutics for the treatment of CNS injury including mitochondrial replacement strategies.
S02: Peripheral Organ Involvement in CNS Trauma 

Chairs: Scott Whittemore, PhD;  University of Louisville & Sonia Villapol, PhD, Georgetown University

  1. Changes in gut dysbiosis and barrier function underlie SCI pathophysiology - Shirish Barve, PhD; University of Louisville 
  2. The effects of TBI on peripheral immune cell responses - Fletcher White, PhD; IUPUI 
  3. Intestional dysfunction following TBI: Lessons from Drosophila - David Wassarman, PhD; University of Wisconsin 

Description

This session will focus on acute and chronic changes in peripheral organ status that detrimentally affect recovery from SCI and TBI. The first speaker will outline the gut-CNS axis and show how changes in the gut microbiome (dysbiosis) and barrier function lead to a worse outcome following contusive thoracic SCI. This pathology derives from acute and chronic inflammation, both peripherally and centrally. He will also delineate the signaling mechanisms involved. The second speaker will discuss acute and chronic liver changes that occur post-SCI and how those changes affect functional recovery. Finally, the third speaker will use a drosophila model of TBI to delineate changes in gut function that underlie the extent to which those flies recover. While some of these data have been published, the majority will be new data. The gut/peripheral organ-CNS axis is emerging as a critical determinate of functional recovery after SCI/TBI. This session will introduce that topic and suggest novel therapeutic approaches that could be readily translated.

Educational Objectives

  1. Relate the interaction between gut and CNS homeostasis.
  2. Describe how gut microbiome load and phyla change rapidly after CNS trauma and have significant impact on functional recovery.
  3. Determine how SCI/TBI results in detrimental affects on peripheral organ function.
S03: Blast-Related Mild TBI- Translational Relevance Starting from the Top (Humans) Down (mechanistic animal models) 

Chairs: David Cook, PhD; University of Washington & Ibolja Cernak, PhD; University of Alberta 

  1. Human Neuropathological Findings of Blast-Related mTBI - Daniel Perl, MD; Uniformed Services University of the Health Sciences 
  2. Behavioral and cognitive symptoms and complex comorbidities of blast-related mTBI in Veterans - Elaine Peskind, MD; University of Washington 
  3. Integration of findings from animal models of blast-induced brain injury to clinical findings - Ibolja Cernak, PhD; University of Alberta
  4. Translational correspondences between animal models and findings in veterans - David Cook, PhD; University of Washington

Description

It is now well-established that blast-related mild traumatic brain injury (mTBI) is associated with a range of significant chronic behavioral and cognitive symptoms that include: memory complaints, irritability, impulsivity, headaches. In addition, a large number of studies have confirmed that individuals with blast-related mTBI display a wide array of abnormal imaging findings as revealed using fluorodeoxyglucose positron emission tomography (FDG-PET), diffusion tensor imaging (DTI), resting and task-based functional MRI, as well as other imaging modalities. Similarly, a growing body data obtained from a wide variety of animal model studies demonstrate that injuries associated with blast or blast-like injuries cause an array of behavioral impairments, pathologic, and neurochemical disturbances in the brain. A critical challenge facing the mTBI research field is to properly wed current and evolving findings from humans with blast-related mTBI, to the neuropathological and mechanistic findings derived from animal model data. By this means, more accurate and translationally relevant inferences can be drawn regarding the underlying structural and functional mechanisms of blast-related mTBI. One well-recognized challenge to achieving this goal involves using carefully designed methods to deliver appropriate battlefield-relevant blast exposures. The significance of this issue is further underscored by recent findings that suggest blast-exposure may give rise to brain injuries with some distinct neuropathological features in blast-exposed Veterans compared to impact-related chronic traumatic encephalopathy. It is equally important that every effort should be made to use information derived from the growing body of findings in blast-exposed humans as the starting place for efforts to craft and refine mechanistic animal models of blast-induced brain injury.

Educational Objectives

  1. Describe the integration of findings from animal models of blast-induced brain injury to emerging clinical findings in individuals with repetitive blast-related mTBI.
  2. Recognize behavioral and cognitive symptoms, as well as the complex comorbidities of blast-related mTBI in Veterans.
  3. Discuss recent human neuropathological findings in cases of blast-related mTBI as they pertain to blast exposure and impact-related mTBI.
  4. Compare the translational correspondences between the neuropathological findings in blast exposed animals to neuroimaging findings in Veterans with blast-related mTBI.
Alpine Dinner & Networking Event 

Description

TBA

Educational Objectives

  1. TBA
  2. TBA
  3. TBA
S'More Collaboration Campfire 

Description

S'More Collaboration Campfire, a modern-day spin on how people have bonded for centuries, is designed to connect and engage attendees in thought-provoking conversations outside of the typical structured business setting.  We are kickin’ it old school with a campfire and s’mores, of course!. If you are new to NNS, looking to make a few new friends or strengthen existing connections, this event is for you!  Open discussion on a variety of topics.

FREE - Open to all Students & Trainees

Educational Objectives

  1. Exchange collaborative ideas for new approaches to neurotrauma
  2. Identify gaps in research and clinical care for neurotrauma
  3. Discuss methods of efficient collaboration in neurotrauma research