Shelley J Russek
Boston University, MA·Neuroscience
Temporal lobe epilepsy (TLE) often worsens over time. After an initial brain injury, molecular changes and rewiring in the hippocampus, a memory center, make spontaneous seizures and memory problems more likely.
- Fields
Neuroscience
Genetics
Pharmacology
- Topics
temporal lobe epilepsy
epileptogenesis
epilepsy progression
- Grants
- 1 known grant, through Apr 2027
What they work on
- Test whether STAT3 signaling in excitatory neurons drives epilepsy progression by silencing synaptic plasticity and neuroinflammation genes, using mice with neuron-specific STAT3 knockout in the intrahippocampal kainate model.
- Map how each hippocampal cell type's genome responds 24 hours and 4 weeks after kainate injury, using multiomics and quantitative molecular imaging in normal and STAT3 knockout mice.
- Identify direct and indirect effects of losing STAT3 in excitatory neurons on both excitatory and inhibitory neurons, using electrophysiology and neuropharmacology.
- Determine how STAT3 signaling in excitatory neurons shapes glial activation by examining the transcriptome and inflammatory markers of microglia and astrocytes.
More about the research
More than 30% of patients do not respond to current drugs, so treatments that stop the disease from progressing are needed. One candidate target is the JAK/STAT pathway, a signaling route involved in inflammation and in how neurons form and strengthen connections. The team previously showed that a STAT3 inhibitor, WP1066, sharply reduced spontaneous seizures in a rat or mouse model of epilepsy. However, blocking the pathway throughout the body or brain could cause side effects. Safer, more targeted therapies require knowing what STAT3 does in each cell type.
Why it matters
Many people with temporal lobe epilepsy have seizures that current drugs cannot control, and their disease can worsen over time. Defining how STAT3 signaling in specific neurons drives that progression could identify cell-type-specific targets, either STAT3 or the genes it controls, for disease-modifying therapies. Such therapies may slow seizures and memory decline with fewer side effects than broad pathway inhibitors.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Detlev Boison
Rutgers University-New Brunswick, NJ·Neuroscience
Test whether blocking adenosine A2A receptors with istradefylline, or activating the astrocyte glutamate transporter GLT-1 with ceftriaxone, prevents epilepsy in the mouse intrahippocampal kainic acid model.
Barna Dudok
Baylor College of Medicine, TX·Neuroscience·Early-career
Test whether CCK and PV basket cells, two types of inhibitory neurons, are active in different brain states in a kainate mouse model of temporal lobe epilepsy, using two-photon calcium imaging with hippocampal field recordings.
Ivan Soltesz
Stanford University, CA·Neuroscience
Identify non-invasive behavioral biomarkers that predict chronic seizures and death, using MoSeq AI analysis of 3D video in mouse models of temporal lobe epilepsy and Dravet syndrome.
The school
Boston University: 26 labs on PI Pages, $784M a year on research, 630 research doctorates a year.
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