University of Washington campus

[Date TBD] Seminar from Dr. Jack Parent

This seminar was originally scheduled for 2020; however, due to health and safety concerns around COVID-19, this talk has been rescheduled for 2021. Check back for updates!

Targeted Augmentation of Nuclear Gene Output (TANGO): A novel therapeutic approach to treat SCN1A-linked Dravet Syndrome

Background:  Targeted augmentation of nuclear gene output (TANGO) is an antisense oligonucleotide (ASO) technology being developed by Stoke therapeutics for the treatment of severe genetic diseases. This ASO therapy targets naturally occurring, non-productive RNA splicing events to restore normal levels of the target protein. In collaboration with Stoke Therapeutics, Dr. Isom has tested this technology in a mouse model of Dravet syndrome.

You Will Need: Dr. Isom will provide an overview of TANGO and present results from testing ASOs in a mouse model of Dravet syndrome.

Speaker Bio: This webinar is presented by Dr. Lori Isom, the Maurice H. Seevers Professor and Chair of the Department of Pharmacology, Professor of Molecular and Integrative Physiology, and Professor of Neurology at the University of Michigan Medical School.

Biological Mechanisms of SUDEP

Background:  Sudden unexpected death in epilepsy (SUDEP) is the most important epilepsy-related cause of death, occurring in at least 1:1000 people with epilepsy each year. The risk of SUDEP increases dramatically in uncontrolled epilepsy. The events leading to SUDEP are thought to be caused by a destabilization of autonomic cardiorespiratory compensatory processes. Dr. Simeone’s research has focused on determining progressive changes in cardiorespiratory function that could increase the probability of SUDEP in preclinical animal models. Identification of temporal biomarkers that can be monitored could lead to opportunities for intervention to postpone or prevent SUDEP.

You Will Learn: Dr. Simeone will discuss the progressive cardiorespiratory dysfunction seen in the Kv1.1 knockout mouse model of SUDEP and the potential role of orexin as a central regulator of SUDEP.

Speaker Bio: This webinar is presented by Dr. Kristina Simeone, Associate Professor and Director of Master’s in Neuroscience Program at Creighton University’s School of Medicine.

What’s New at the ETSP?

Background:  The NINDS Epilepsy Therapy Screening Program (ETSP), is a preclinical screening program that provides researchers the opportunity to screen potential therapeutic agents in established rodent seizure models. Since its establishment, the ETSP has played a role in the development of several FDA-approved epilepsy drugs.

You Will Learn:  This webinar will broadly discuss the scope of the ETSP and new models and assays available at the University of Utah.

Speaker Bio:  This webinar is presented by Dr. Cameron Metcalf, a Research Assistant Professor in Pharmacology and Toxicology at the University of Utah. He is also a Co-Investigator and the Associate Director of the Anticonvulsant Drug Development Program.  Dr. Metcalf’s primary research interests include the evaluation and advancement of novel therapies for the treatment of epilepsy and pain.

Status Epilepticus: 2019 Update

This talk will:

  • Define Status Epilepticus, its clinical stages, and treatment
  • Discuss the Ictal-Interictal Continuum
  • Apply new monitoring techniques

Stay tuned – additional details are coming soon.

Astrocyte Dysfunction Contributes to the Development of TBI-Induced Epilepsy

For years, scientists have focused on neuronal damage as the cause of neurological disorders, such as epilepsy. A growing body of evidence shows that impaired astrocyte function happens before seizures manifest.

Traumatic brain injury (TBI) is a primary cause of epilepsy, which is characterized by scar formation that seals off injured areas from healthy brain tissue. These scars are formed by astrocytes. Scars inhibit normal function and have been associated with seizure genesis.

Researchers modeled TBI in mice, using a weight drop injury paradigm, in order to determine whether astrocyte scar formation is involved in TBI-induced epilepsy. While animals developed epilepsy, no scars formed, but astrocytes behaved atypically, with decreased protein expression and decoupling with brain vessels. There were also more atypical astrocytes in epileptic animals. These data support the hypothesis that altered astrocyte function contributes to the development of TBI-induced epilepsy.