To the brain, cf the blood brain barrier. Not smart. Just trying...

To the brain, cf the blood brain barrier. Not smart. Just trying to make sense of the announcement and the cause of action of afam with PD.

"The program objectives are to determine whether afamelanotide – through melanocortin-1 receptor (MC1R) activation – is able to lower α-synuclein (a toxin) in blood levels in PD patients, and positively affect neurons of the midbrain. MC1R is known to be a key receptor in brain and skin cells."

Since afamelanotide is known to optimise the function of the MC1R, it is hypothesised that the drug treatment would have a positive effect in PD by lowering α-synuclein, as recently demonstrated in preclinical studies.

At the heart of the problem in Parkinson’s lies the loss of dopamine producing neurons in the brain due to toxicity caused by α-synuclein.

There is now evidence that afamelanotide – by binding to MC1R – could maintain stability and integrity of the affected neurons and slow down progression of the disorder.