Founded in 2024, Legacinetics is bridging the gap between cutting-edge laboratory breakthroughs and real-world patient outcomes.
Legacinetics has a targeted approach to address one of the largest human health burdens globally, Alzheimer’s Disease, for which no cure exists. The latest research shows that diseases like Alzheimer’s are dynamic, "multi-channel" afflictions rooted in metabolic dysfunction and chronic inflammation. Uniquely, the Legacinetics technology has been established to address these systemic drivers, concurrently. By moving beyond traditional cell therapies and mesenchymal-derived approaches to exosome technology, we have unlocked a way to deliver potent regenerative signals to the brain, and broader metabolic pathways — overcoming the safety, scalability, and delivery limitations that have held the field back for decades.
Legacinetics was founded in 2024 with a singular focus: to commercialize transformative, cell-free therapies for the world’s most challenging neuroinflammatory and metabolic conditions. The team at Legacinetics are bridging the gap between cutting-edge laboratory breakthroughs and real-world patient outcomes, starting with a new frontier in Alzheimer’s treatment.
Mesenchymal stem cells (MSCs, including iPSC-derived, bone-marrow, umbilical-cord, or adipose sources) actprimarily via paracrine signalling, mitochondrial transfer, and immunomodulation rather than direct neuronalreplacement – providing multi-channel impacts to address multi-channel disease pathways concurrently.
MSC’s have been proven to address multiple AD pathways simultaneously (supported by dozensof successful preclinical studies and early clinical signals, e.g., laromestrocel) without the furtheradvancement of the Legacinetics technology.
MSCs upregulate Aβ-degrading enzymes (neprilysin/NEP, IDE) and enhance microglial phagocytosis; APOE2/3-edited MSCs further improve lipid handling and reduce aggregation-prone cargo in EVs
MSCs reduce tau hyperphosphorylation (via GSK-3β inhibition, galectin-3, reduced oxidative stress) and enhance proteasomal/autophagic clearance; secretome factors lower p-tau levels.
MSCs promote synaptogenesis (^synaptophysin, PSD-95) via BDNF/GDNF/VEGF and thrombospondin-1; mitochondrial transfer rescues synaptic bioenergetics.
MSCs reprogram microglia from M1 (pro-inflammatory) to M2 (phagocytic/anti-inflammatory) via TSG-6, TGF-β, GDF-15, sICAM-1; reduce TNF-α/IL-1β/ROS while increasing IL-10/Arg1. Strongest and most replicated MSC effect.
MSCs donate functional mitochondria via EVs/tunneling nanotubes (CD38/cADPR-dependent in some contexts); restore ATP, reduce ROS, activate PGC-1α. NAD+- preserving edits (e.g., PARP1/NNMTKO) amplify this.
MSCs preserve BBB integrity (TIE2 signaling, reduced leakage), promote angiogenesis (VEGF), and repair neurovascular unit; improve cerebral blood flow and waste clearance.
MSCs exert broad anti-inflammatory and metabolic reprogramming (NAD+ elevation, senescence reduction, SASP modulation); systemic IV effects reset peripheral inflammation that feeds brainpathology.
MSCs counteract senescence-associated secretory phenotype (SASP), restore youthful transcriptomic profiles via miRNAs and trophic factors; early intervention (preclinical) slows aging-like changes.
MSCs inhibit NLRP3 inflammasome, reduce senescence markers (p16, SA-β-gal), and secrete anti-senescence factors; NAD+-boosting edits directly counter senescence-driven NAD+ depletion.
