Apoaequorin Neuron Preconditioning for Reduced Inflammation

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Solution Overview

Problem

There is a need for new and alternative therapeutics to treat neuronal inflammation with reduced side effects, particularly in the context of ischemic stroke, as existing treatments like NMDA receptor blockers have failed in clinical trials and pose undesirable side effects.

Innovation Solution

Apoaequorin-containing compositions are administered to precondition neurons, reducing neuronal inflammation and TNFα protein levels through oral or injection methods, including nutraceutical formulations.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If NMDA receptor blockers are used to treat neuronal inflammation, then neuroprotection is achieved, but undesirable side effects such as hallucinations and coma occur

Engineering Contradiction:
Improveneuroprotection efficacyVSAvoidside effects
Core Design Contradiction:
ReliabilityVSObject-affected harmful factors

Solution Approach 1:

The patent extracts and utilizes calcium binding proteins (calbindin, parvalbumin, calretinin) as separate therapeutic agents from the NMDA receptor blocking mechanism. These CaBPs are administered to bind and buffer cytosolic calcium directly, achieving neuroprotection through a different molecular pathway that avoids the side effects of NMDA receptor blockers

Inventive Principle:
Principle #2Taking out (Extraction)

Solution Approach 2:

Calcium binding proteins serve as intermediary molecules that mediate calcium homeostasis without directly blocking NMDA receptors. They act as buffer intermediaries that control cytosolic calcium levels through binding and release mechanisms, providing a safer therapeutic approach

Inventive Principle:
Principle #24Intermediary (Mediator)

2Reliability

If calcium binding proteins are administered to prevent calcium toxicity, then neuroprotection is achieved, but the treatment complexity increases

Engineering Contradiction:
ImproveneuroprotectionVSAvoidtreatment complexity
Core Design Contradiction:
ReliabilityVSDevice complexity

Solution Approach 1:

The patent describes compositions that can contain multiple calcium binding proteins (calbindin, parvalbumin, calretinin) that work through a common mechanism of calcium buffering. This multi-functional approach allows a single composition to address various aspects of calcium dysregulation simultaneously, simplifying the treatment protocol while maintaining effectiveness

Inventive Principle:
Principle #6Universality (Multi-functionality)

Solution Approach 2:

The patent emphasizes administering calcium binding proteins before an ischemic insult occurs, allowing the proteins to be present and ready to buffer calcium when the insult occurs. This preliminary action simplifies the treatment by preventing the need for complex post-insult interventions

Inventive Principle:
Principle #10Preliminary action

Applied Scientific Principles

This section explains which scientific principles are used to turn an abstract innovation direction into a practical engineering solution.

Function Achieved in This Case

Apoaequorin provides neuroprotection by reducing neuronal inflammation and TNFα levels, improving mental and physical health with minimal side effects.

Implementation Method 1

apoaequorin, a calcium binding protein... apoaequorin has been found to be useful in preconditioning neurons in a subject to reduce subsequent neuronal inflammation

Methodology Applied
Scientific EffectCalcium binding: Absorption (physical)

Data Source

PatentUS20250367254A1Apoaequorin-Containing Compositions and Method of Using Same to Treat Neuronal Inflammation
Publication Date: 2025.12.04 STILLWATERS BIOSCIENCE GROUP LLC
  • US20250367254A1 patent drawing
  • US20250367254A1 patent drawing
  • US20250367254A1 patent drawing

AI summary

The present invention is directed to methods of preconditioning neurons to reduce neuronal inflammation in a subject. Such methods include a step of administering apoaequorin to a subject, wherein the subject's neurons are preconditioned to reduce subsequent neuronal inflammation in the subject.