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An interaction between parkin and its substrate -synuclein is a crucial regulatory component of dopaminergic neuron degeneration, loss-of-function mutations in PARK2 usually cause early-onset autosomal recessive PD (Kitada et al., 1998), whereas disease-associated mutations in -synuclein are usually associated with autosomal dominant PD (Polymeropoulos et al., 1997)

Dopamine supplementation would be evident, but this hydrophilic neurotransmitter does not cross the BBB and cannot enter the CNS due to brain endothelial tight junctions, active brain endothelial metabolism and lack of transporters [5]

What if the real issue is that most approaches target symptoms while ignoring what's actually happening at the cellular level

Is Cagrilintide better than semaglutide alone