Evyatar Swissa
I spent a decade learning how the brain breaks. Now I help build a platform to fix it.
Director of In-vivo Research, Modulight Bio · Research Associate, Weizmann Institute · PhD, Ben-Gurion University
Turning a receptor into a dimmer switch
At Modulight Bio I direct in-vivo research on an optogenetic therapy. The platform uses optoGPCRs: light-activated G protein-coupled receptors delivered to the nerves that carry pain. Our workhorse is eOPN3, a rhodopsin borrowed from mosquitoes that recruits the Gi/o cascade and suppresses neurotransmitter release at the presynaptic terminal.
It does not force a neuron to fire, and it does not clamp it silent. It turns down what that terminal releases, and then lets it come back on its own. The first indication we are taking towards the clinic is trigeminal neuropathic pain, where the nerve is reachable enough for light to do the work.
The control in the corner is that mechanism, not a toggle. Hold it and the model goes quiet. Release it and the suppression decays on its own, the way a bistable opsin does.
Why it breaks, what fixes it, and how a fix reaches a patient
One interface asked about three ways: the barrier between blood and brain, and the neurons whose excitability depends on it.
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Why it breaks
Friedman lab · Ben-Gurion UniversityAnimal models of epilepsy and status epilepticus, following what happens in the weeks after the seizures stop. Blood-brain barrier pathology in the right place predicted which animals would become epileptic months later, accurately enough to serve as a biomarker. Treating early prevented the damage and the epilepsy alike.
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What it does when nothing is wrong
PhD · Ben-Gurion UniversityThe same barrier, asked about in a brain that is not injured. Sustained sensory activity opens the microvessels of the cortex that receives it, and that opening travels with long-term synaptic plasticity. We saw it in rats, then in people.
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Getting a fix to a patient
Modulight Bio · Weizmann InstituteAn optogenetic therapy taken from a construct towards the clinic: delivery, implant design, chronic behavioural testing, and the preclinical evidence a regulator will read.
The short version
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BSc, Chemistry
Ben-Gurion University of the Negev -
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Research assistant
Experimental Neurosurgery · Ben-Gurion University -
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MSc, Brain and Cognitive Sciences
Ben-Gurion University of the Negev -
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PhD, Brain and Cognitive Sciences
Blood-Brain Barrier lab · Prof. Alon Friedman -
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Director of In-vivo Research
Modulight Bio -
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Research Associate
Weizmann Institute
Written down
- Paroxysmal slow waves mark ictal networks Epilepsia · Boyer-Aymé, Imtiaz, Prager, Swissa et al.
- Cortical plasticity is associated with blood-brain barrier modulation eLife · Swissa, Monsonego, Yang et al.
- Craniotomy for acute monitoring of pial vessels in the rodent brain MethodsX · Aboghazleh, Alkahmous, Swissa et al.
- PVP-coated Gd-grafted nanodiamonds as a novel and potentially safer contrast agent for in vivo MRI Magnetic Resonance in Medicine · Panich, Salti, Prager, Swissa et al.
- Midazolam and isoflurane combination reduces late brain damage in the paraoxon-induced status epilepticus rat model NeuroToxicology · Swissa, Bar-Klein, Serlin et al.
- TMS-induced controlled BBB opening: preclinical characterization and implications for treatment of brain cancer Pharmaceutics · Vazana, Schori, Monsonego, Swissa et al.
- Blood-brain barrier dysfunction in status epilepticus: mechanisms and role in epileptogenesis Epilepsy & Behavior · Swissa, Serlin, Vazana, Prager, Friedman
- Paroxysmal slow cortical activity in Alzheimer's disease and epilepsy is associated with blood-brain barrier dysfunction Science Translational Medicine · Milikovsky, Ofer, Senatorov, … Swissa et al.
- Imaging blood-brain barrier dysfunction as a biomarker for epileptogenesis Brain · Bar-Klein, Lublinsky, Kamintsky, … Swissa et al.
- sec-Butyl-propylacetamide (SPD) and two of its stereoisomers rapidly terminate paraoxon-induced status epilepticus in rats Epilepsia · Bar-Klein, Swissa et al.
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