Pharmaceutical Agents Mimicking Time-Restricted Feeding
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Solution Overview
Problem
Current methods for time-restricted feeding (TRF) are difficult to follow and the underlying molecular mechanisms are not fully understood, making it challenging to replicate its anti-aging benefits without adhering to a strict feeding schedule.
Innovation Solution
Administering agents that mimic the effects of TRF by targeting and modulating specific proteins such as UNC-51-like kinase (ULK1), adenosine monophosphate protein kinase (AMPK), microtubule-associated protein light chain 3 (LC3), and ribosomal protein S6 kinase beta-1 (S6K) to activate or inhibit them, thereby enhancing circadian-regulated autophagy, which can extend lifespan and healthspan.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Duration of action of stationary object
If time-restricted feeding is implemented to extend lifespan and healthspan, then longevity benefits are achieved, but compliance difficulty increases
Solution Approach 1:
The patent extracts the essential molecular mechanism (autophagy activation) from the complex behavioral intervention (time-restricted feeding schedule). By identifying that TRF works through activating autophagy via specific proteins like AMPK and ULK1, the invention isolates this core mechanism and targets it directly with pharmaceutical agents, eliminating the need for patients to adhere to restrictive feeding schedules while preserving the longevity benefits
Solution Approach 2:
The patent introduces pharmaceutical agents as intermediaries that mediate between the desired outcome (autophagy activation) and the patient. Instead of requiring patients to directly engage in time-restricted feeding behavior, small molecule compounds serve as intermediaries that activate the same molecular pathways (AMPK, ULK1, LC3) that TRF would normally stimulate, thereby achieving the same biological effect through a more convenient route
2Duration of action of stationary object
If time-restricted feeding schedule is followed to activate circadian-regulated autophagy, then healthspan is extended, but lifestyle complexity increases
Solution Approach 1:
The invention extracts the beneficial molecular effect (circadian-regulated autophagy activation) from the complex lifestyle intervention (time-restricted feeding). By identifying the specific proteins and pathways involved (AMPK, ULK1, LC3), the patent isolates this mechanism and targets it with pharmaceutical agents, thereby eliminating the need for complex scheduling while maintaining the healthspan extension benefits
Solution Approach 2:
The patent changes the parameter of intervention from behavioral (feeding time restrictions) to biochemical (pharmaceutical agent administration). This parameter change transforms the intervention from something requiring behavioral compliance and temporal planning into a simpler medical treatment that can be administered independently of the patient's daily schedule, thereby reducing lifestyle complexity
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
This approach allows for the extension of lifespan and healthspan without the need for a time-restricted feeding schedule, demonstrating that targeting specific proteins can activate circadian-regulated autophagy, delaying aging and improving healthspan.
Implementation Method 1
the underlying molecular mechanisms, including the pathways and proteins which are targeted by time-restricted feeding... proteins adenosine monophosphate protein kinase (AMPK) and ribosomal protein S6 kinase beta-1 (S6K) were targeted by the time-restricted feeding
Implementation Method 2
the increase in lifespan and healthspan was due in part to the activation or increase in circadian-regulated autophagy. The proteins which were involved in this process included Drosophila Atg1 and Atg8, which correspond to human UNC-51-like kinase (ULK1) and microtubule-associated protein, light chain 3 (LC3)
Data Source
AI summary
The present disclosure relates to methods and compositions for increasing or extending lifespan and/or healthspan and/or delaying aging using agents which mimic the effects of time-restricted feeding and/or activate or enhance circadian-regulated autophagy. In particular, the present disclosure relates to increasing certain proteins including UNC-51-like kinase (ULK1), adenosine monophosphate protein kinase (AMPK) and microtubule-associated protein, light chain 3 (LC3), and decreasing other certain proteins including ribosomal protein S6 kinase beta-1 (S6K) protein in order to increase lifespan and/or healthspan and delay aging.