Yes skint, I somehow missed that. It is in fact little hidden IMO: "The findings showed that PBT434 passed the blood-brain barrier and inhibited the alpha-synuclein protein which when aggregated in the brain is a pathological hallmark of Parkinsonian conditions and is considered an important biologic target for treating these neurodegenerative diseases".
So this inhibition by PBT434 was seen in healthy humans (but how??) but aggregation inhibition in the animal models (IMO). However, when there is less alpha-synuclein, it's aggregation is also inhibited. But it is difficult to see aggregation inhibition in clinical examination or in CSF analysis which are difficult to interpret ( as the paper above tells). However, the comparison between the PBT434 treated and placebo-treated may have been helpful.
In any case, this announcement is very positive but perhaps it could have been much more clear and tell a bit more clearly how important the finding was when now planning phase2 study, most likely the only study needed for PBT434 to become an orphan drug for MSA. The good excuse is that this was a financial statement, however.
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- PBT434 inhibits alpha- synuclein in the brain.
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