For Medical Professionals

Our Techology

Pioneering neuroplasticity-based treatments that restore neural connectivity and adaptive capacity for sustainable mental healthy recovery

Neural Plasticity

Depression stems from impaired adaptability in prefrontal cortex, hippocampus, and amygdala networks.

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.

Neuroplasticity in Depression

Explore the paradigm shift from monoamine hypothesis to neuroplasticity-based understanding of depression etiology and treatment mechanisms.

  1. Our technology delivers precise 60 Hz light stimulation through the eyes.
  2. This signal propagates through neuronal circuits across different brain regions, ultimately activating the brain’s immune cells.
  3. These immune cells, called Microglia, begin to get activated and reshape the protective layer surrounding neurons.
  4. This allows for the formation of new, healthy neural connections, while gradually reducing existing harmful ones.

1) Retinal light delivery at 60 Hz

Haven delivers therapeutic light stimulation through the eyes in the form of 60 Hz flickering light. This rhythmic light signal is delivered via the retina and transmitted along the optic nerve into the brain.

Eye with optic nerve receiving 60 Hz light

2) Network entrainment

Through a process called entrainment, neuronal networks across the brain begin to oscillate in sync with the 60 Hz light pattern.

Neural Entrainment

3) Plasticity is limited by PNNs

In the adult brain, plasticity is limited by perineuronal nets (PNNs). These dense structures enwrap inhibitory interneurons and restrict synaptic remodeling.

Neuron surrounded by perineuronal net
Passive microglia drifting around neuron

4) Remodeling reopens plasticity

PNN remodeling reopens a window for plasticity. This structural change enables the formation of new synaptic connections and restores juvenile-like plasticity in the adult brain.

Neuron without perineuronal net
Active microglia remodeling around neuron

5) Target disorders of impaired plasticity

This treatment mechanism can be used to target disorders involving impaired neuroplasticity, such as depression, anxiety, and PTSD.

Clinical Applications

Our Science

Depression is a complex and heterogeneous disorder arising from genetic vulnerability, early life adversity, chronic stress, and neurobiological alterations. The neuroplasticity hypothesis offers a comprehensive framework for understanding and treating depression.

For decades, the monoamine hypothesis has shaped our understanding of depression, proposing that deficits in serotonin, norepinephrine, or dopamine underlie its pathophysiology. While this theory led to the development of widely used antidepressants, it fails to explain their delayed therapeutic onset and limited efficacy.

In recent years, the neuroplasticity hypothesis has emerged as a more comprehensive framework. It posits that depression stems from impairments in the brain's ability to adapt to experience, rewire neural circuits, and form new connections. The drug ketamine has brought this pathway to the forefront, through its rapid antidepressant effect as a transient blockade of NMDA, which triggers a cascade resulting in rapid synaptogenesis and reversal of stress-induced synaptic deficits within hours.

Ketamine's efficacy supports the idea that restoring neuroplasticity, rather than simply correcting neurotransmitter imbalances, is key to treating depression.

Overcoming current medication limitations

However, while SSRIs are limited by slow onset, modest efficacy, and significant side effects such as insomnia, nausea, or reduced libido, ketamine also faces important constraints. It requires repeated administration, commonly via infusion or nasal spray, leading to strong side effects such as confusion, dissociation, and impaired coordination, necessitating frequent treatments under close clinical supervision.

Decoding the Electrical Signal

The brain isn't just a chemical system. It's also an electrical one. It communicates using pulses of electricity, like signals sent along a wire. At the Institute of Science and Technology Austria (ISTA), Syntropic's co-founding team discovered that with pulsed light it is possible to send the brain a unique electrical "morse code". This signal directs microglia, the brain's immune cells, to restructure the Perineuronal Nets (PNNs) surrounding neurons, allowing new neuronal connections to grow, much like what occurs during early brain development. These findings revealed a new mechanism of action for flickering light in restoring neuroplasticity.

Light-Based Revolution

Syntropic Medical has discovered a novel, non-invasive, non-pharmacological way to remodel the PNN and induce neuroplasticity. This approach uses 60Hz intermittent white light stimulation delivered directly to the eyes through a wearable device. This light pulse promotes PNN remodeling by engaging the brain's natural entrainment processes.

Brain Entrainment

By recording brain activity with electrodes, Syntropic researchers observed that flickering light stimulation leads neurons to produce in response rhythmic waves of activity at around 60 Hz, in a phenomenon known as entrainment. This refers to the synchronization of brainwave activity with an external rhythmic stimulus, observed across multiple regions of the brain. Over time, this synchronization gradually decreases, reflecting an adaptive increase in neuroplasticity, the brain's capacity to reorganize, form new connections, and adapt to stimuli.

We aim to provide a practical, mechanism grounded option for patients with depression by restoring circuit flexibility. As evidence accumulates, we will share detailed protocols and training for clinicians interested in incorporating plasticity based care.