RESEARKA

The geroscience hypothesis posits that interventions targeting core aging mechanisms could simultaneously prevent or delay multiple age-related pathologies, offering a strategic alternative to the one-drug-one-disease paradigm that has dominated pharmaceutical development. Under this framework, AGEs have been proposed as both a mechanistic driver and a tractable intervention target, because AGE formation is modifiable through dietary restriction, pharmacological inhibitors, and potentially existing approved agents with off-target anti-glycation properties. Evidence from preclinical models suggests that reducing AGE accumulation may attenuate vascular stiffening, improve insulin signaling, and preserve stem cell differentiation capacity (Xu 2023), yet the question of whether these laboratory findings translate to meaningful human healthspan gains has not been resolved. The appeal of repurposing existing compounds—such as agents that may interfere with AGE formation or crosslinking—lies in their established safety profiles and regulatory familiarity, though the specific mechanisms by which AGE interventions achieve benefit in humans remains incompletely characterized. Whether the geroscience framing adequately captures the complexity of AGE biology or instead oversimplifies a context-dependent phenomenon is a question this synthesis aims to address.

Citation Support

• source_1 Movahedian 2025
• source_2 Kopytek 2025
• source_3 Chang 2025
• source_4 Wu 2025
• source_5 Li 2026