Neural Plasticity
Depression stems from impaired adaptability in prefrontal cortex, hippocampus, and amygdala networks.
Our Techology
Pioneering neuroplasticity-bsed treatments that restore neural connectivity and adaptive capacity for sustainable mental healthy recovery
Rapid Action
Syntropic enables a faster therapeutic effect compared to standard antidepressants, which generally require 2 to 3 weeks to start taking effect.
Precision Treatment
Moving beyond monoamine rebalancing to restore network function and synaptic connectivity.
Novel Mechanism of Action
- Our technology delivers precise 60 Hz light stimulation through the eyes.
- This signal propagates through neuronal circuits across different brain regions, ultimately activating the brain’s immune cells.
- These immune cells, called Microglia, begin to get activated and reshape the protective layer surrounding neurons.
- This allows for the formation of new, healthy neural connections, while gradually reducing existing harmful ones.
The Paradigm Shift: From Monoamines to Neuroplasticity
Traditional Monoamine Hypothesis
- Depression = chemical imbalance (serotonin, norepinephrine, dopamine)
- Focus on neurotransmitter rebalancing
- Limited explanatory power for delayed effects
- Doesn't address treatment resistance
Modern Neuroplasticity Hypothesis
- Depression = impaired neural adaptability
- Focus on synaptic connectivity and circuit function
- Explains rapid ketamine effects
- Addresses network-level dysfunction
The Foundation: Glutamatergic Neurotransmission
- Glutamate, the brain's primary excitatory neurotransmitter, modulates synaptic strength and plasticity through NMDA and AMPA receptors.
- In depression, glutamate signaling is often dysregulated, leading either to excitotoxicity or synaptic underactivation.
- The rapid antidepressant effects of NMDA receptor antagonists such as ketamine have brought this pathway to the forefront.