In several papers it's been hypothesised that there is leakage in the BBB in PD patients and other neurodegenerative diseases (coming back to the notion that vascular issues underlie the causes of these diseases. But you're right, afa should not be able to cross the BBB because it isn't a cyclic peptide ie bremelanotide. I've been wondering what is the mode of action for treating PD if the drug can't get to where it's supposed to go? We know stroke can be treated outside the BBB by restoring the integrity of the BBB and reducing inflammation through vascular action. I just surmised that this might be how they intended to treat PD.
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