Soccertese, your points are valid points. Though, they can all be discussed:

- they test them all the time in vitro and on mice/rats:

And they found lots of things being neuroprotective on mice and rats but not on humans. That's why they should redo these things on these new human neurons. Things like Creatine, Isadiprine, Azilect, ... it is easy to test them on these human neurons and this would lead to much better insight into whether they are neuroprotective or not. At least you can show whether they are definitely not neuroprotective so you don't need to waste resources on them.

- people taking all pd meds continue to get worse, that seems to tell me pd drugs are not very neuroprotective:

That doesn't mean these things are not neuroprotective. Neuroprotectiveness means that it slows down neuronal death. It doesn't mean it will stop neuronal death completely. So still, al these meds could be neuroprotective. And testing this on human neurons could at least tell us whether they are not.

If some med doesn't show neuroprotectiveness at all on these human neurons, then we can almost say with 100 % guarantee that these meds are not neuroprotective. I would really like to see how Azilect does on these neurons. We are having these complicated studies now on a huge amount on patients which take years to see if Azilect is neuroprotective or not. Now, we could finally know it within 6 months if we would test it on these human neurons.

- coq10 had a major neuroprotective study, there is a new one:

I don't believe these studies. You have different kind of people with their own type of PD. Some progress fast, others slow. They do not make a distinction of this during the trials, mainly of course because they have no clue how to make this distinction. As a simple example, suppose you have an extreme case in which everyone in the group that gets the med has a fast progressive PD form, and in the placebo group you have all slow progressive PD patients ... your study results will be completely wrong. The med might have slowed down the progression of the first group significantly but it hasn't been slowed down more than the people in the placebo group that had a slow progressive form of PD. I realize this is an extreme example, but because these clinical trials usually don't consist of enough people, something similar could occur and lead to wrong conclusions.

As you could see from the article of the OP, coQ10 is neuroprotective; while the initial study claimed it could not be proven coQ10 to be neuroprotective. The problem is in the design of the experiments in clinical trials. The only way such trials will detect neuroprotectiveness is if the neuroprotectiveness is incredible.

- major problem is by the time you are diagnosed, you have lost supposedly 80% of your dopamine neurons:

I don't remember the website, but it is a big and important Parkinson website where I found it. I remember the titles and subtitles of this site are in green colour ... maybe someone knows this website ... but I read on it that last year one of the researchers found out that this 80 % is wrong. There are much more neurons available when first diagnosed than currently believed.

- I think the major problem is not the amount of subjects (though it is an important subject) but the fact there are no biomarkers. Even if you have lots of people with PD in trials ... so what ? You can't even measure how they progress.