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[1] At the cellular level, the tendon work is genuinely mechanistic: in cultured rat tendon fibroblasts, BPC-157 accelerated cell outgrowth, improved survival under oxidative stress, and increased migration in a dose-dependent way, apparently through the FAKpaxillin pathway

Understanding the mechanism helps explain why its effects are so broad

This entails determining the prevalence of cognitive and mental comorbidities, determining the degree of motor impairment, and conducting neuroimaging studies to validate the existence of distinctive brain abnormalities linked to PD