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Mutations in either gene impair this surveillance, allowing damaged mitochondria to persist and propagate oxidative stress ( 2.2 Mitochondrial dysfunction and oxidative stress Mitochondrial complex I deficiency is consistently observed in PD, leading to impaired ATP synthesis and overproduction of reactive oxygen species (ROS) ( Furthermore, LRRK2 mutationsparticularly G2019Sare linked to disrupted mitochondrial dynamics, altered kinase activity, and aberrant autophagy ( 2.3 Ferroptosis: iron-mediated cell death Ferroptosis is an emerging mechanism in PD, characterized by iron-dependent lipid peroxidation
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The increase of Langerhans cells in the hindpaw skin is thought to cause the loss of IENFs due to the local production of neurotoxic pro-inflammatory cytokines (Wang et al., 2012)
How long is the cycle for BPC-157
