"With three different lines of clinical research exploring intracellular inhibition of the aggregation of the [alpha-synuclein] protein via small molecules, we will hopefully see some clarity on the role that this protein plays ..."
scienceofparkinsons.com/202...
But note that the word "see" does not have the word "soon" in front of it.
Thanks for sharing
Are you Clement Rick or Clemen Trick?
A-Syn deaggregators are many, blueberries / anthocyanins, Mannitol, Melatonin, Ambroxol, Bacillus Subtilis, many more.
None have shown benefits.
Which begs the question, is misfolded A-Syn aggregates the cause or consequence of PD?
Yes, this is a very interesting question. If the alpha synuclean turns out to be a result of Parkinson’s and not the cause, there goes decades of research wasted looking down the wrong rabbit hole.
Whatever theory we come up with, it must take into account the lesson learnt from familial PD, that too much alpha-syn, in itself, can cause PD.
At this point there is plenty of evidence that alpha synuclein is the cause. See, for example, this study:
pubmed.ncbi.nlm.nih.gov/256...
"A53T human α-synuclein overexpression in transgenic mice induces pervasive mitochondria macroautophagy defects preceding dopamine neuron degeneration "
Again, this is a mice study.
If a-syn was the cause, then Ambroxol, which expels a-syn from the brain (mice study), or Mannitol, which dissolves a-syn agrregates, should at least stop progression, of PD, if not cure it
Just a correction, a-synis not harmful, misfolded a-syn aggregation and entanglement is thought to be the cause of PD
Another interesting theory about water and light, and protein folding inside cells. Maybe that is the resson why light therapy benefits PD.
It is the same mechanism but in PD, protein is misfoded.
Start at 6:20 mark if interested
When it comes to evaluating treatments for disease, animal models are but one step in the process. On the other hand, when it comes to interventional experiments to evaluate causes of disease, animal models are the end of the line. That, in conjunction with observational studies of humans, has to suffice for understanding the causes.
As it happens Ambroxol has been reported in a human study and mannitol have been reported by PWP to improve their condition.
“What the investigators found in through their analysis was that the time to dopaminergic therapy was shorter for those with baseline depression compared to those without depression, suggesting that the presence of mild depression in early Parkinson’s is associated with needing dopamine therapy earlier. And this finding applied to those individuals who were also taking an antidepressant”
So they reason the tricyclics antidepressant prevent PD when compared with ssri and eg mirtazapine but I feel it is the other way around. I think people that have depression and it is treated with ssri and eg mirtazapine but not tricyclics antidepressants have their PD symptoms exascerbated.
For my husband it certainly seemed the antidepressants were the cause of the symptoms and if you look at their side effects on the drug specs it lists a whole lot of PD symptoms. I know now I have totally got him off all the antidepressants he is better than he had been for many years, way before his diagnosis. (He also started a few new supplements at the same time the antidepressants were completely stopped).
So my opinion is not that the tricyclics ones prevent PD, but the others bring it on. Although that doesn’t tie in with their observation alpha synuclein breaks down with the tricyclics one I suppose.
Low Protein with Mucuna
Molecular chaperones for removing misfolded AS
Parkinson's Disease: emerging treatment target, the NLRP inflammasome. 
Experiences with fast protein digestion 
Do animal proteins cause an increase in alpha synuclein? 
