Special Interest Groups


SIG: Basic Mechanisms and Neuroscience: Tauopathies and Epileptogenesis: Cause or Correlation?

Convention Center, Room 322
7:00 AM-8:30 AM
Behavioral Health Providers

Neurological disorders with increased burden of phosphorylated Tau, e.g. Alzheimer's Disease, are characterized by neuronal hyperexcitability and elevated lifetime risk of seizures. Vice versa, recent work suggests that reducing Tau burden in animal models of epilepsy decreases neuronal excitability and inhibits seizures. These studies suggest that drugs targeting Tau could be therapeutic in epilepsy. Despite this progress in the field, the underlying mechanisms are unclear, and it is controversial if Tau hyperphosphorylation is cause or consequence of seizures, or both. This proposed SIG will shed light on these questions by discussing the most current basic research on Tau in epilepsy. Speakers will provide different perspectives on the topic. Dr. Swami Thippeswamy will discuss how deletion of Tau or Fyn affects seizure onset and epileptogenesis in response to chemoconvulsants. Dr. Bret Smith will present data showing how epileptogenesis affects Tau hyperphosphorylation in a mouse model of acquired temporal lobe epilepsy and what the impact of hyperphosphorylated Tau is on seizure susceptibility, epileptogenesis, and hippocampal neuron excitability. Dr. Lori Isom will present research suggesting that the role of Tau may not be generalizable to genetic epilepsies. Talks will be short to allow for engagement and discussion among speakers and the audience.

Coordinators: Christina Gross, PhD and Joaquin N Lugo, PhD

Speakers: Bret N. Smith, PhD; Lori L. Isom, PhD; and Thimmasettappa (Swamy) Thippeswamy, DVM, PhD