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Developing a Novel Treatment for a Novel Target
new direction
Traditional depression treatments don't work for everyone- it's time to go back to the drawing board to reexamine the problem. Let's evaluate and integrate what we know about the neurobiology of depression to fix your brain.
Things that benefit brain health
Let's start by thinking about what goes on in your brain. Your neurons, or brain cells, make up a network of circuits that hosts the software of your mind. It's very much like a computer.
Healthy software relies on healthy hardware. How can we fix our brain hardware? Let's think about the things shown to benefit brain health:
High intensity exercise
Adequate sleep
Intermittent fasting
Mental stimulation
Positive social enrichment
Stress reduction
the Root cause
What's the mechanism behind these brain-boosters?
BDNF!
Brain-derived neurotrophic factor (BDNF) is a protein in your brain that helps to keep your neurons alive and healthy. These brain-boosters have been shown to increase BDNF activity.
Increase BDNF activity
Greater survival, protection, and connectivity of neurons
Brain-derived neurotrophic factor (BDNF) is a key molecule modulating mood, motivation, learning, and memory
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Interference with BDNF signaling is linked to psychiatric conditions including depression, bipolar disorder, and cognitive disturbances in traumatic brain injury.
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BDNF is decreased in Major Depressive Disorder and increased after chronic treatment with traditional antidepressants.
Aingeal is developing a novel class of therapeutic agents that increase the activity of BDNF to to strengthen synaptic connections to fix your neuronal "hardware."
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Ketamine isn't perfect. Despite its therapeutic value, it carries risks of abuse, dissociation, and cognitive interference. Thus, our mission is to develop a treatment that safely and rapidly increase BDNF action to alleviate depression.
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Recently, ketamine was approved for depression that resists conventional treatment. Ketamine is an NMDA receptor blocker that boosts BDNF activity and produces rapid antidepressant effects.
We found that the synaptic scaffold protein PSD-95 is required for the activation of TrkB, the high affinity receptor for BDNF.
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We have designed novel peptidomimetic drugs (Syn class) that bind to PSD-95 to enhance BDNF signaling and exert potent anti-depressant effects.
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These compounds have all the advantages of peptide-based drugs (high potency and activity, low toxicity), while small enough to cross the blood-brain barrier.
