Jamie Maguire
Tufts University, MA·Neuroscience
People with epilepsy face a risk of sudden unexpected death in epilepsy (SUDEP), a leading cause of epilepsy-related death whose causes remain unclear. The lab found that mice engineered to have overactive stress circuits die of SUDEP more often.
- Fields
Neuroscience
Physiology
- Topics
epilepsy
stress
HPA axis
- Grants
- 1 known grant, through Nov 2027
What they work on
- Test whether activity in the pathway from stress-hormone CRH neurons in the hypothalamus to the brainstem's nucleus of the solitary tract is increased in chronically epileptic mice at risk of SUDEP.
- Determine whether chemogenetically activating this CRH stress pathway is sufficient to increase SUDEP incidence in epileptic mice.
- Examine whether stress-circuit overactivity raises SUDEP risk by exaggerating cardiac vagal output, the nerve signaling that slows the heart, during challenges to normal body balance.
- Test whether chronic stress, an environmental driver of hyperactive stress circuits, impairs cardiac vagal function and increases SUDEP risk in mice.
More about the research
Related hormone abnormalities were seen in patients who died of confirmed or suspected SUDEP. Both stress and SUDEP involve brain circuits that control heart rate and breathing. This project asks whether an overactive stress system pushes these control centers into dangerous patterns.
Why it matters
SUDEP is a devastating outcome for people with epilepsy and their families. Identifying overactive stress circuits and abnormal heart-slowing nerve signals as contributors could reveal risk factors and possible targets for preventing SUDEP. Because chronic stress is part of the hypothesis, the work may also show how environmental stress raises risk. The mechanism may be relevant to other forms of sudden death.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Eric Krause
Georgia State University, GA·Neuroscience
Determine how HPA stress-axis activity reduces weight-loss quality, including muscle loss, during treatment with GLP-1 receptor agonists such as semaglutide, using a CRF-neutralizing antibody (Anti-CRF) in mice.
Christopher Del Negro
William & Mary, VA·Neuroscience
Test whether inhibitory GABAergic neurons of the central amygdala connect directly to excitatory breathing-rhythm neurons in the preBötzinger complex, using light-activated (optogenetic) proteins in VgatCre mice and recordings from brainstem slices.
Yumei Feng Earley
University of Rochester, NY·Neuroscience
Test whether (pro)renin receptor (PRR) signaling in tyrosine hydroxylase-positive neurons of the hypothalamus (THPVN neurons) impairs glucose balance, using neuron-specific targeting and wireless blood glucose monitoring in mice.
The school
Tufts University: 19 labs on PI Pages, $278M a year on research, 144 research doctorates a year.
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