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So that was how we actually started looking at a hypothesis for Alzheimer's and Parkinsons

BPC-157 is typically associated with nitric-oxide signaling networks and angiogenic pathway regulation, while TB-500 contributes actin-regulated cellular migration and structural reorganization mechanisms [1][6][10][11]

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These new findings encourage a novel working hypothesis for further research, that a chemical-modification mechanism enables transformation of HGF through interaction or reaction with LASSS under physiological conditions, resulting in the retention of HGFs biological activity after exposure to peroxynitrite, at least until an enhanced form of HGF undergoes metabolic turnover in vivo