Bailey Gwyn – Interdisciplinary Researcher, Musician, Advocate, and Creator of Audia™ AI

Bailey Gwyn is an interdisciplinary researcher, neuro-inspired AI developer, and disability rights advocate. He is the creator of Audia™ AI, a self-evolving, context-aware assistant designed to support people with chronic illness, neurodivergence, and disability. His work bridges systems medicine, education law, functional genomics, and ethical technology design.

Areas of expertise include Ehlers-Danlos syndrome (EDS), systems biology, hyperthymesia, accessibility innovation, and education rights advocacy. Bailey’s research and advocacy focus on building inclusive technologies that improve healthcare access, empower patients, and advance disability justice.

Official website: https://baileygwyn.xyz | Location: North Carolina, USA

Bailey Gwyn

Back

Effects of THC (Tetrahydrocannabinol)

Neuroprotection refers to preserving the structure and function of neurons—limiting damage, degeneration, or death. In conditions like Alzheimer’s, Parkinson’s, MS, and after traumatic brain injury (TBI), neuroprotection is a key therapeutic goal. Below are the primary mechanisms studied for THC’s potential neuroprotective actions.

1) Antioxidant Properties

Reduction of oxidative stress

Excess free radicals damage neurons and contribute to neurodegeneration. THC demonstrates antioxidant activity that can help neutralize reactive species and reduce oxidative load in neural tissue.

  • May limit lipid peroxidation and protect neuronal membranes.
  • Has been reported to exhibit antioxidant capacity comparable to or exceeding some classical antioxidants in preclinical work.

2) Modulation of the Endocannabinoid System (ECS)

Endocannabinoid receptor activation (CB1 / CB2)

The ECS regulates mood, pain, immune signaling, and neuronal survival. THC activates CB1 and CB2 receptors distributed across the CNS and peripheral tissues.

  • CB1 (brain): Linked to synaptic plasticity, neurogenesis, and pro-survival signaling—may mitigate damage from inflammation or excitotoxicity.
  • CB2 (immune/microglia): Dampens neuroimmune activation and inflammatory cascades that can injure neurons.

3) Reduction of Neuroinflammation

Anti-inflammatory effects in the CNS

Chronic neuroinflammation accelerates neuronal injury in many neurodegenerative disorders.

  • THC acting at CB2 can reduce microglial activation and inflammatory mediator release.
  • Lowering inflammatory tone may support neuronal function and slow disease progression.

4) Protection Against Excitotoxicity

Prevention of overstimulation and neuronal death

Excess glutamate → calcium overload → cell death. This pathway underlies injury in multiple neurological conditions.

  • THC may modulate glutamatergic transmission and reduce hyperexcitability.
  • Helps preserve the neurotransmitter balance required for neuronal survival.

5) Stimulation of Neurogenesis

Promotion of new neuron growth

Preclinical studies suggest THC can promote neurogenesis in memory-related structures (e.g., hippocampus), potentially supporting plasticity where degeneration impairs cognition.

  • May aid repair/regeneration and help counter cognitive decline.

6) Traumatic Brain Injury (TBI)

Neuroprotection following injury

After TBI, inflammation, oxidative stress, and cell death drive secondary damage.

  • Animal models indicate THC can reduce neuroinflammation and neuronal loss, supporting functional recovery.

7) Potential Cognitive Effects

Cognition in neurodegenerative disease

Beyond cytoprotection, some studies report improvements in cognition or memory under disease conditions; findings are mixed and context-dependent.

  • In Alzheimer’s models, THC has been associated with improved spatial memory and performance measures.

8) Multiple Sclerosis (MS)

Reducing neuroinflammation & spasticity

MS involves immune-mediated demyelination and neuroinflammation.

  • CB2-mediated immunomodulation may lower inflammatory injury.
  • Clinical use of cannabinoid-based therapies has been associated with reduced spasticity and symptom relief in some patients.

Important: Evidence spans preclinical to early clinical studies; larger, well-controlled trials are needed to define efficacy, dosing, safety, and indications. THC can have psychoactive effects and drug–drug interactions. Work with a qualified clinician—especially if you have cognitive or psychiatric conditions.

Accessibility