Calcium-Release Stabilizing Molecules for Alzheimer's Disease

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Solution Overview

Problem

Current treatments for Alzheimer's disease are hindered by the complexity of its pathological mechanisms, leading to a need for agents that can stabilize calcium release in brain cells to address calcium dysregulation and related cognitive decline.

Innovation Solution

Administration of calcium-release stabilizing molecules such as polypeptides, polynucleotides, or small molecules that target ryanodine receptors and inosital triphosphate receptors in brain cells, including FKBP1a, FKBP1b, junctophilin 3, and calmodulin 3, to reduce or reverse calcium dysregulation.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Adaptability or versatility

If multiple pathological factors and mechanisms are addressed simultaneously, then comprehensive treatment coverage is improved, but treatment complexity and difficulty increase

Engineering Contradiction:
Improvetreatment coverageVSAvoidtreatment complexity
Core Design Contradiction:
Adaptability or versatilityVSDevice complexity

Solution Approach 1:

The patent segments the complex AD pathology into a primary target (calcium dysregulation) that can be addressed with a specific class of molecules (calcium-release stabilizing molecules), separating this from other pathological factors. This allows focused treatment on the most critical mechanism while acknowledging other factors exist but are not simultaneously treated.

Inventive Principle:
Principle #1Segmentation

Solution Approach 2:

Instead of attempting to treat all pathological factors simultaneously (the conventional approach), the patent inverts the strategy by identifying and treating a specific downstream effect (calcium dysregulation) that results from multiple upstream pathological processes. This reverse approach simplifies treatment while still addressing the functional consequences of AD pathology.

Inventive Principle:
Principle #13The other way round (Inversion)

2Reliability

If calcium dysregulation is stabilized, then cognitive function is improved, but the mechanism complexity increases

Engineering Contradiction:
Improvecognitive functionVSAvoidmechanism complexity
Core Design Contradiction:
ReliabilityVSDevice complexity

Solution Approach 1:

The patent extracts the calcium release stabilization function from the complex web of AD pathology. By using molecules that specifically stabilize calcium release from intracellular stores (ryanodine and inositol triphosphate receptors), the invention isolates and treats the calcium dysregulation component, making the therapeutic mechanism simpler and more direct despite the underlying complexity of AD.

Inventive Principle:
Principle #2Taking out (Extraction)

Data Source

PatentUS9464322B2Methods for diagnosing and treating alzheimer's disease (AD) using the molecules that stabilize intracellular calcium (Ca<sub>2+</sub>) release
Publication Date: 2016.10.11 UNIVERSITY OF KENTUCKY RESEARCH FOUNDATION
  • US9464322B2 patent drawing
  • US9464322B2 patent drawing
  • US9464322B2 patent drawing

AI summary

The subject technology relates, in part, to a method of treating Alzheimer's Disease (AD), early-stage AD, elevated risk of AD, mild cognitive impairment (MCI), or other forms of age-related cognitive decline in a subject in need thereof by administering to the subject a molecule that promotes calcium-release stabilization in ryanodine receptors (RyRs) and/or inosital triphosphate receptors (InsP3Rs) in brain cells. Diagnostic methods using calcium-release stabilizing immunophilins, junctophilins or calmodulin are also disclosed.