Queuine Neuroprotection for Mitochondrial Dysfunction
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Solution Overview
Problem
Current treatments for Parkinson's disease, primarily relying on L-DOPA administration, induce several unwanted side-effects and do not effectively address the underlying mitochondrial dysfunction associated with the disease.
Innovation Solution
The use of queuine, a precursor or derivative thereof, or its analogues, as a pharmaceutical compound to prevent or treat mitochondrial dysfunction-related diseases, including Parkinson's disease, by providing neuroprotective effects.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If L-DOPA administration is used to treat Parkinson's disease, then dopamine concentrations are increased and motor symptoms are improved, but unwanted side-effects occur including end-of-dose deterioration, on/off oscillations, freezing during movement, dyskinesia, and drug resistance
Solution Approach 1:
The patent introduces mitochondria-protective compounds as intermediary substances that address the root cause of Parkinson's disease (mitochondrial dysfunction) rather than directly replacing dopamine. These compounds act as mediators between the dysfunctional mitochondria and the dopaminergic neurons, providing neuroprotection and reducing reliance on L-DOPA, thereby minimizing side-effects while maintaining treatment effectiveness
Solution Approach 2:
The patent employs compounds that prevent mitochondrial dysfunction before it leads to neuronal death. By administering mitochondria-protective agents that stabilize mitochondrial function and prevent oxidative stress, the treatment addresses the disease process in advance, reducing the need for high-dose L-DOPA and subsequent side-effects
2Duration of action of moving object
If chronic L-DOPA administration is used to maintain dopamine levels, then motor symptoms are managed, but drug resistance develops and treatment efficacy decreases over time
Solution Approach 1:
The patent changes the fundamental parameter of treatment from dopamine replacement (L-DOPA) to mitochondrial protection. This parameter change addresses the underlying cause of drug resistance by preserving neuronal health and mitochondrial function, allowing for sustained treatment effectiveness over longer durations without the diminishing returns observed with chronic L-DOPA use
3Quantity of substance
If L-DOPA is administered to cross the blood-brain barrier and increase dopamine, then dopamine deficit is corrected, but the blood-brain barrier limitation requires high doses that increase side-effects
Solution Approach 1:
The patent uses mitochondria-protective compounds as intermediaries that can cross the blood-brain barrier more effectively than L-DOPA. These compounds directly protect dopaminergic neurons and improve mitochondrial function within the brain, achieving dopamine deficit correction through neuroprotection rather than dopamine replacement, thereby reducing the need for high doses and associated side-effects
Data Source
AI summary
The present invention relates to a compound of the following formula (A): or a pharmaceutically acceptable salt or hydrate thereof, for use in the prevention or treatment of a disease associated with a mitochondrial dysfunction.