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In a transected rat sciatic nerve model (Gjurasin et al., 2010, published in Regulatory Peptides), BPC-157 promoted functional nerve reconnection and accelerated axonal sprouting, with treated animals recovering motor function significantly faster than controls
Thus, the etiology of primary cerebral folate deficiency includes the presence of autoantibodies against the folate receptor (FR1) and mutations in the FOLR1 gene, which encodes the FR1 protein [101]
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