Neuro-Restorative Cognitive Protocol

Introduction

This protocol represents a biphasic approach to treating Age-Related Cognitive Decline (ARCD) and executive dysfunction pathologies such as ADHD and early-stage neurodegenerative diseases such as Alzheimer’s, Lewy Body Dementia, and symptoms of Parkinson’s.  Unlike traditional stimulant therapies which temporarily mask symptoms, this regimen utilizes a 2-phased approach to rebuild neural and synaptic systems while solidifying new neuronal patterns leveraging Cognitive Behavioral Therapy (CBT).

Phase 1 focuses on aggressive synaptogenesis, mitochondrial restoration, and dendritic branching to physically rebuild neural architecture.  The appropriate CBT protocol should be initiated prior to the start of Phase 1 to ensure the patient has the tools to apply what they have learned while forming new neuronal and synaptic systems.  While specifics for the appropriate CBT protocol is out of scope for this article, the focus should be on solidifying the tools they’ve gained through CBT in a safe environment that does not discourage when mistakes are made.

Phase 2 leverages this heightened neuroplasticity to solidify behavioral patterns through CBT.  The patient’s CBT protocol should be tailored to their needs, lifestyle, and the progress of the disease.  While the appropriate CBT protocol for each patient’s needs are out of scope for this article, the focus of each session during this phase should prioritize affirming what they’ve learned so far.  The addition of NA-Semax-Amidate and NA-Selank-Amidate is to utilize a window of enhanced neuroplasticity and resilience during CBT sessions.

Successfully executing this protocol requires strict adherence to dosing windows to balance Brain-Derived Neurotrophic Factor (BDNF) elevation with inhibitory control.  Otherwise, patients may experience excitotoxicity, severely limiting functional gains and the long-term potentiation of this protocol.  If patients following this protocol experience anxiety and/or excitotoxicity effects during Phase 1, anxiolytics and/or an additional dose of L-Theanine can be added to mitigate these effects; however, with a proper low-to-moderate fat diet and adherence to the protocol, these effects should be fully mitigated.

Phase 1: Weeks 1-4

The following protocol is to be administered for a strict 4-week cycle to induce structural remodeling.  Details and links to the specifics of each compound are provided below:

• Dihexa: An angiotensin IV analog that exhibits potent neurogenic activity by stimulating dendritic branching and synaptogenesis via the HGF/c-Met pathway to effectively increasing the available neurons and synaptic pathways.
• P21: A synthetic mimetic of Ciliary Neurotrophic Factor (CNTF) that directs neural stem cells to mature into functional neurons rather than glial scar tissue by working synergistically with Dihexa to densify the neural network.
• J-147: A curcumin derivative developed to treat the aging brain that targets mitochondrial ATP synthase to restore cellular energy production and reduces neuro-inflammation, providing the metabolic energy required from the rapid neuronal growth triggered by Dihexa and P21.
• Noopept: A peptide-mimetic that improves signal-to-noise ratio and sensory gating via acetylcholine and AMPA receptor sensitization.  This allows for immediate improvements in focus while supporting NGF and BDNF expression.

Phase 2: Weeks 5+

These agents are introduced after the structural repair phase to prime the brain for learning during therapeutic intervention.

• NA-Semax-Amidate: An ACTH fragment that rapidly elevates BDNF and modulates the dopaminergic system.  Used specifically prior to CBT, it creates a “plasticity window” that enhances the retention of new coping strategies and organizational skills.
• NA-Selank-Amidate: An anxiolytic peptide that modulates GABA and inhibits enkephalin degradation.  It reduces the stress response often associated with cognitive exertion or therapy, facilitating a state of “relaxed focus.”

Continuous Metabolic & Inhibitory Support

These compounds must be taken daily throughout both Phase 1 and Phase 2 to ensure substrate availability and prevent excitotoxicity.

• Alpha-GPC: A rapid-acting choline donor that provides the acetylcholine precursor necessary to sustain the high-velocity signaling induced by Noopept and Semax, preventing cholinergic depletion headaches.
• Magnesium L-Threonate: The only form of magnesium that’s been proven to elevate brain magnesium levels, which prevents the potential for excitotoxicity during synaptogenesis caused by the upregulation of NMDA receptors.
• L-Theanine: An amino acid that promotes Alpha-wave production to regulate excitatory signaling when paired with Magnesium L-Threonate.

Protocol Dosing Schedule

Potential Risks & Mitigation Strategies

Ideal Candidate Profile

This protocol is indicated for patients presenting with subjective age-related cognitive decline (ARCD), early-stage memory impairment, or executive dysfunction disorders such as ADHD (Inattentive Type).  Ideal candidates are those who are motivated to engage in active cognitive behavioral therapy (CBT) alongside pharmacological intervention.  Patients must be screened for history of seizures, active malignancy (due to angiogenic properties of Dihexa), and mania (as the excitatory nature of the stack could exacerbate bipolar pathology).

Conclusion

The Neuro-Restorative Cognitive Protocol offers a targeted intervention for the aging or dysregulated brain.  Physicians can maximize the structural benefits of regenerative peptides while minimizing the risks of excitotoxicity.  Success relies on the continuous administration of the metabolic and inhibitory support agents (Alpha-GPC, Magnesium Threonate, and L-Theanine) to maintain the delicate homeostatic balance required for healthy neuroplasticity.  Additionally, research has shown that increasing EPA and DHA can also have lasting effects on neurodegenerative disorders as well.