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However, this type of A-induced overstimulation of neurogenesis, when occurring in the early stages of development, has been claimed to be responsible for serious disturbances in adult neurogenesis by reducing the number of available neural progenitors

The mechanism likely involves the same angiogenic pathway: bone repair is acutely dependent on vascularization of the fracture gap, and BPC-157's VEGF-stimulating activity addresses this bottleneck directly

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