Prothena reports 97 % reduction of alpha synuclein after 1 dose!
 

Progress in reducing alpha synuclein but another year has gone by!

Prothena Reports Results from Phase 1b Study of PRX2 Demonstrating Robust Antibody CNS Penetration and Significant Reduction of Free Serum Alpha-synuclein in Patients with Parkinson's Disease (NASDAQ:PRTA)

Zanpar, assuming everything checks out in phase 2 and 3, how many years would it take before it might be available? Would neurons be restored, or is this drug only going to halt or slow down PD progression? Is this drug our best hope in your opinion?

The Prothena drug seems to be quite promising as it reduces the alpha synuclein protein that the prevailing science seems to be believed to be the protein that is gumming up the works and causing Parkinson's. Whether AS causes parkinsons and other questions like - do we need some alpha snuclein or how much is too much seem to be yet to be answered. I'm no expert but it seems like phase 2 will happen next year and hopefully phase 3 in 2018. I think studies of the drug Nilotinib are quite promising too and at least 3 studies of this drug are slated to be started in the New Year! Further, it is a drug that has been used for at least 8 years. It increases autophagy which seems to clear alpha snuclein. If the alpha synuclein theory is true I believe we're going to see vast and exciting advances in the next few short years!

At 5 Years, Nilotinib Offers Benefit Over Imatinib in CML | Cancer Network

Everyone has Alpha Synuclein but it is misfolded in Parkinson's patients.

Parkinson's Disease | Podcast: Parkinson's Common Denominator -- A Sticky Protein

Eli Lilly’s Experimental Alzheimer’s Drug Failed in Large Trial
 

An experimental Alzheimer’s drug that had previously appeared to show promise in slowing the deterioration of thinking and memory has failed in a large Eli Lilly clinical trial, dealing a significant disappointment to patients hoping for a treatment that would alleviate their symptoms.

The failure of the drug, solanezumab, underscores the difficulty of treating patients who have reached the point of showing even mild dementia, and supports the idea that by that time the damage in their brains may already be too extensive. And because the drug attacked the amyloid plaques that are the hallmark of Alzheimer’s, the trial results renew questions about a leading theory of the disease, which contends that it is largely caused by amyloid buildup.

http://www.nytimes.com/2016/11/23/he...rial.html?_r=0

This result was disappointing, although not surprising. It's important for PWP because, conceptually, solanezumab (a monoclonal antibody) works the same way that the anti A-Syn vaccines work. It just targets a different protein, Amyloid. There are probably a lot of reasons why the drug failed (tau may be the appropriate target, not amyloid; the patients may have been too far progressed, etc). However, we need to keep in mind that when we see early trial results from Prothena, AffiRis and Proclara that show reduction of A-syn. You still have to prove that reducing cerebral fluid levels of the protein will actually lead to improvement in symptoms and slowing or stopping the progression. We still have a long way to go.

Do you know how many months the study was done? After decades of buildup of plague I doubt if 6 months or shorter will have any effect.

This trial was for 76 weeks. There were actually three different phase 3 trials with over 2,000 patient volunteers. It was a huge study and Lily was very hopeful for success. The stock was hit hard on this news. The hope is that the failure was due to attacking the wrong protein, which is very likely as there has been a big change in AZ research since 2010, when this all got started. Today, the focus is much more on Tau rather than amyloid. There are also people who think that the drug would only work if it is started very early in the course of the disease. There was improvement for people who took the drug, but it wasn't statistically significant, or practically relevant. Data mining deeper may show that it works for some groups, particularly younger, newly DXed.

I'm in no way trying to put a damper on this type of research. I still believe that currently, it's our best hope (even more than Nilotinib). I just wanted to remind everyone that lowering a-syn levels, as it appears the three companies we are following can do, does not mean they will slow or stop PD progression. That still needs to be proven.