i've been looking at the phase1 data, does anyone see anything strange in this130week graph, page-6

the phase2 trial has shown there was no affect from the NTCELL so yes, any increase in pd symptoms as manifested by the decrease (less negative) in UPDRS scores would be a reduction in placebo affect. that increase in pd symptoms in week 108(?) and then a significant decrease after week 108, going from -3 to -12 just sticks out like a sore thumb and i would like to see the individual data. did only 1 patient have a terrific benefit (#1) and the other 3 continue the trend of getting worse at week 130?

since a lot of people lost a lot of money because LCT seemed so confident that the benefit observed in phase1 was not due to placebo, i'm just questioning how they made sure patients were truly OFF during the UPDRS scoring and why there was such big swings in scores, it makes me question the data a little. another example:
https://www.otcmarkets.com/ajax/showNewsReleaseDocumentById.pdf?id=17712
page 12. PART III

i copied the graph data into a table


…...w4...w12...w20..w26...w42..w58.
Pt1 0 -1 -7 -17 -7 -13
pt2 -12 -7 -7 -11 -10 -12
pt3 -13 -6 -8 -2 -6 no data
pt4 - 7 -8 --2 -8 -7 no data


observations
1. patient3 and patient4 got very little benefit.
2. why did the scores decline from week 26 to week42 except for patient3 who got better? Just the normal variation in the UPRDS scoring method?
3. at week 58 i find it hard to believe patient's 1 and 2 had almost the same score.

finally, dr. snow was not ignorant of the significant placebo affect of drilling a hole in a pd'ers head, at a NZ PD ASSOCIATION presentation he gave he showed slides of an earlier study using pig cells and the results were just like LCT's, very large benefit in phase1 that lasted 1 year and a failed phase2. they had a ballpark figure from that phase1 trial as to the placebo affect yet they downplayed it in all their communications regarding their phase1 trial imho



1. goto 30minutes, DR. SNOW discusses earlier clinical trials where something is injected thru a hole in a patients head to stimulate nerve growth or create new neurons.
a. earlier trials
1. adrenal tissue transplants – didn't work
2. transplanted midbrain from aborted fetuses. PET scan showed more dopamine producing cells after the
procedure some patients were essentially cured, others had severe side affects. Not a simple treatment,
Dr. Snow stated he doesn't think it will become a treatment but mentioned there was new research on this procedure.
He made the point that in this treatment, it was proven that some patients got significantly better and stayed
better so it wasn't fruitless to try other types of transplants. This study proved that transplanted cells can survive
in a human brain indefinately if you have the RIGHT TISSUE.
3. the pig brain is very similar to a human brain so lets try transplanting pig fetus brain cells. And this is where SNOW
reveals he knows a lot about the placebo affect. Pay attention. Quoting Dr. Snow:
“We transplant pig heart valves into humans, why not try fetus pig brain cells? That's ok in theory but in practice
the system rejects foreign tissue. But when they did the study it looked like the patients improved.
(stop the video at 35minutes 52seconds 35:52 )
Look at the graph showing the results of the first clinical trial which was not blinded or placebo controlled, the
same design as LCT'S phase1 trial. It's a graph of:

AVERGAGE TOTAL UPRDS IMPROVEMENT FROM BASELINE, MEASURING BOTH OFF (UNMEDICATED)
AND ON STATES (MEDICATED)
Boy,. Those results look mighty impressive, an avg. improvement in TOTAL UPRDS of about 12points starting in
MONTH3 and lasting at least 12 months and if you squint real hard you can see the notes below the graph. Which
say “12patients, 6:CyA, 6: graft treated with MHC class 1AB”
“ No SAEs” (NO SERIOUS ADVERSE EVENTS)
“No PERVs” (No Porcine Endogenous Retroviruses
) “2 patients with > 50% improvement on UPDRS”
“no change in FD PET” a technique using MRI and radioactive tracers to measure the size of dopamine
producing areas in the brain. Having no change implies that any benefit detected in the treatment group
was due to something other than increased production of dopamine. GEEZ, in this study 2 PATIENTS\
had >50% improvement yet no change in dopamine was measured in any patient and that gets almost
zero discussion about maybe it might be …..... THE PLACEBO AFFECT!!! There was an increase in
dopamine in the successful fetal cell transplants and an autopsy of a patient who died of natural causes
showed that the fetal cells had lived. AND some of the patients in the fetal cell trial developed
dyskinesias, involuntary movements - michael j. fox has dysk. - which is caused by too much dopamine
yet there were no increase in dyskinesias in any of the phase1 patients and I think at the AGM it was
asked if any drug regimes were changed in any of the phase2b patients and the answer was no, they stayed
with the same drug regime during the trial.
i apologize if i made any mistakes here. again, my concern is how well did they ensure phase1 patients were OFF during the UPDRS scoring and how did they account for patients getting better then worse then better after week26, makes me wonder, was it just due to the inherent variation in their UPDRS scoring proficiency?

And finally there is CAROL. No disclaimer in her video about potential placebo affect. She is telling viewers how much better she is but why no before and after video or even a video if her walking around? And no videos of the other 3 patients. Maybe they wanted their confidentiality.