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Matthew Weston, Ph.D.

Matthew Weston, Ph.D.

Associate Professor

Matthew Weston, Ph.D.

"We’re examining the genes, cells, and critical time points in development that influence synaptic changes underlying epilepsy to find new, targeted therapies.”


Seeking solutions to childhood seizure disorders

How do certain genetic variants cause severe epileptic disease?

Recent next-generation DNA sequencing efforts in humans have uncovered a handful of genes in which loss- or gain-of-function variants cause severe neurodevelopmental disorders called developmental epileptic encephalopathies (DEEs). DEEs are characterized by unremitting, treatment-resistant seizures and intellectual disability. The fact that these DEE-causing variants cause severe epileptic disease suggests that they are exceptional cases that overcome the brain’s innate plasticity mechanisms. Matt Weston seeks to understand how and why these genetic variants cause such an extreme imbalance of excitation and inhibition in the brain. His premise is that this work will advance understanding of normal physiological processes, delineate disease mechanisms, and point toward novel therapeutic strategies.

  • Associate Professor, Fralin Biomedical Research Institute at VTC
  • Associate Professor, School of Neuroscience, College of Science, Virginia Tech

McCabe, MP, Shore, AN, Frankel, WN, & Weston, MC (2021). Altered fast synaptic transmission in a mouse model of DNM1-associated developmental epileptic encephalopathy. eNeuro, 8(2), ENEURO.0269-20.2020. 

Shore, AN, Colombo, S, Tobin, WF, Petri, S, Cullen, ER, Dominguez, S, Bostick, CD, Beaumont, MA, Williams, D, Khodagholy, D, Yang, M, Lutz, CM, Peng, Y, Gelinas, JN, Goldstein, DB, Boland, MJ, Frankel, WN, & Weston, MC (2020). Reduced GABAergic neuron excitability, altered synaptic connectivity, and seizures in a KCNT1 gain-of-function mouse model of childhood epilepsy. Cell Reports, 33(4), 108303. 

McCabe, MP, Cullen, ER, Barrows, CM, Shore, AN, Tooke, KI, Laprade, KA, Stafford, JM, & Weston, MC (2020). Genetic inactivation of mTORC1 or mTORC2 in neurons reveals distinct functions in glutamatergic synaptic transmission. eLife, 9, e51440. 

University of Vermont, Robert Larnder, M.D., College of Medicine, Assistant Professor

Baylor College of Medicine, Postdoctoral Fellow

Baylor College of Medicine, Postdoctoral Associate

  • Baylor College of Medicine, Ph.D., Neuroscience
  • University of Virginia, B.A., Echols Interdisciplinary Studies, concentration in Writing, English, German
  • Professor John J. Trentin Scholarship award for Outstanding Coursework, 2005
  • Rush and Helen Record Neuroscience Fellowship for Outstanding Graduate Student at Baylor College of Medicine, 2007-2008
  • Coming Together on Epilepsy Genetics Meeting, Travel Award Jackson Labs, Bar Harbor, ME, 2011
  • Fellow, NIH-NINDS Brain Disorders and Development Training Grant, 2010-2012
  • Epilepsy Foundation Postdoctoral Research Fellowship, 2013-2014
  • American Epilepsy Society Young Investigator Workshop Invited Speaker and Travel Award, 2014
  • Citizens United for Research in Epilepsy (CURE) Young Investigator Travel Award GRC, 2014
  • K99 Pathway to Independence Award, NIH/NINDS, 2014