PAG Labs Research Briefing

The science behind structural skin aging.

Facial aging is not only a surface problem. PAG Labs frames dermal aging as a systems-level failure involving NAD+ decline, sirtuin suppression, senescent fibroblast accumulation, and collagen glycation.

Core pathway
NAD+ SIRT1/SIRT3 MMP-1 control

The protocol targets collagen loss upstream, before visible surface change becomes permanent.

The biology

Three failure modes converge inside the dermis.

After midlife, NAD+ availability declines, sirtuin activity drops, and MMP-1 collagenase becomes harder to suppress. At the same time, senescent fibroblasts secrete inflammatory SASP signals, while glycation stiffens collagen and elastin fibers.

01

NAD+ depletion

NAD+ is required for sirtuin signaling, mitochondrial repair, inflammatory control, and collagenase regulation.

02

Senescent fibroblasts

Damaged fibroblasts remain metabolically active and release SASP signals that accelerate matrix breakdown.

03

AGE cross-linking

Advanced glycation end-products make collagen rigid and difficult to remodel, even when new collagen is produced.