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Harvey Singers new article

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I didn't get to read the while study but I'm not buying it. Who's to say those are the antibodies that are even causing the damage? Read this by Dritan Agillou. He's the scientist who has proven what cells are crossing the BBB and how they get there. If you scroll down you'll get to the part about pandas. His research is currently undergoing peer review and will hopefully be published within the next 6 months. It should change everything! A and by the way, its TH17 cells that are infiltrating the BBB.



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I wonder what lab ran the samples?? I don't think it's Dr. Cunningham's b/c she would have also tested for anti-lysoganglioside and anti-D1. This is what Singer tested for "N-acetyl-beta-d-glucosamine, tubulin, and the dopamine 2 receptor." I also think if it was Cunningham's lab there would have been something in there about Cam kinase ll?


I also think he's using the same sample of kids (pulled from the Tourette Study group) from the 2008 Pediatrics article. He had 40 (or 44?) PANDAS kids for that one too. And it was longitudinal. I'm guessing he took a bunch of blood samples from this group of kids and got multiple "PANDAS" studies out of them.

Edited by eamom
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I have to say, I am always so impressed (NOT!) when a paper authored by someone (in this case, Singer), constantly refers back to previous papers by the self-same author (Singer), as though those references offer some sort of impartial support or corroboration! :angry:


ChrissyD was kind enough to forward me a full copy, and I count no less than 9 such references. Reminds me of a similar nay-sayer paper authored by Stanford Shulman in which he repeatedly quoted himself from previous papers.


I guess the pressure to publish is such that these guys have to keep doing it, even if they have nothing new to say. <_<

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Yes, this is the exact same group as the 2008 Pediatrics article, where the purported PANDAS kids didn't actually have PANDAS, and one of the lead author's (Leckman) even admitted this to the Boston Globe. Singer/Kurlan have used data from this non-pandas group in MULITPLE papers with the aim of refuting PANDAS.
"Serum samples were available from 44 subjects with the diagnosis of
PANDAS. Individuals were participants in a longitudinal Tourette Syndrome
Study Group multicenter study of streptococcal infection and
exacerbations in children with tics and obsessive–compulsive symptoms
(Kurlan et al., 2008)."
Also, the labs were NOT run by Cunningham:

"Methodology is a modification of Lopez and Schnaar (2006).Assays
of antigen (10μg/ml; N-acetyl-D-glucosamine conjugated to bovine
serum albumin (BSA), GlcNAc, Dextra Laboratories; purified bovine
brain tubulin, MP Biomedicals; or human dopamine D2 receptor,
PerkinElmer) were incubated overnight at 4 °C, then washed with
0.1% Tween in phosphate buffered saline (PBS). Plates were blocked
with 1% BSA, washed, and incubated with serum diluted 1:500 in PBS
with BSA. After washing, plates were incubated with secondary anti-
(Sigma). Optical density values were measured
at 405 nm on an automated Bio-rad (Hercules, CA) Model 680
Microplate Reader and corrected by blanks (antigen without serum).
Assays were performed in duplicate. All assays were performed in the
laboratory of Dr. Harvey Singer at the Johns Hopkins Hospital."
This paper is a bunch of garbage and I suspect even Harvey Singer knows that.
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I was able to get the full text article. As with other work by this author and colleagues, the abstract does NOT represent the details in the study.


Here is my take on the study:


Singer took blood samples from the kids from the Kurlan study to test for changes in streptococcal, tubulin, and dopamine receptor 2 antibodies (no - there is no mention of Cam Kinase II in the article).


We have to remember that this group of kids received throat cultures every month to check for strep and also had blood tests every few months to check for strep. If the kids had strep, their pediatricians were notified and pediatricians were allowed to put them on antibiotics if they wanted to - but no one actually measured who went on antibiotics.


Also, this many children in this study were on medications to supress tics and manage OCD symptoms and they remained on those medications throughout the study - so we really don't know if they missed exacerbations because the symptoms were suppressed.


Furthermore, the kids in this study had relatively few changes in OCD during exacerbation - as opposed to the kids in Swedo's first 50 cases.


Now - here is my take on this article


Singer and colleagues had 44 kids with PANDAS - of those, 19 were in exacerbation at the time of the blood draw (as determined by a clinician in the Kurlan study).


He had 40 kids with Tourette - of those 13 were in exacerbation, 27 were not in exacerbation at the time of the blood draw.

He had 24 kids who were just typically-developing kids.


He ran Elisa assays based on a modification of Lopez and Schnaar (2006) procedure. I really don't know anything about assays, but the Cunningham (2006) article used a different method for their analysis, so I wonder if the method itself can lead to some differences in findings.


When he did his analysis, he used non-parametric statistics. Cunningham used a combination of parametric and non parametric. Parametric statistics actually make it more likely that you will find difference between the groups; non parametric statistics are less robust and make it less likely that you will see differences. However, you really need larger sample sizes for parametric statistics... so the point here is that just the type of statistic alone could make a difference in the outcome.



1. Antitubulin - they actually found that kids with TS in exacerbation were significantly higher than those who were not inexacerbation. However, kids with PANDAS in exacerbation were not significantly higher than those who were not in exacerbation. However, he then compared the TS kids in exacerbation with controls and those not in exacerbation with controls and reports there was no difference. So... the take home message here is that the kids with TS actually showed increased tubulin binding when in exacerbation as opposed to not in exacerbation.


2. Table 2 looked at tics, OCD, and ADHD symptoms and compared kids with PANDAS who had an exacerbation with a strep infection to those who had an exacerbation without a strep infection. Interestingly, of all the children having exacerbations in both groups - only tics increased consistently. 6/12 had increases in OCD with the exacerbation, and only 3/12 had increases in ADHD. So - this is the question about the Kurlan study all together - were these really PANDAS kids (with only 1/2 of them having OCD increases) and, if so, were they really in exacerbation?


3. Anti -D2 - no significant differences were seen among the groups, although the PANDAS kids showed some differences between those in exacerbation and those not in exacerbation, but it was not significant at .061 (.05 or lower is significant).


4. N-acetyl-beta-d-glucosamine (GlcNAc)- For this test, the kids with PANDAS overall were actually significantly LOWER than both TS and controls, and the binding was higher in PANDAS kids in exacerbation than those not in exacerbation. Since the overall binding was lower than controls, they dismissed it. I really don't know how to interpret this. Perhaps someone else out there knows more about this test.


So that is my take on this study. I am hoping Cunningham will chime in at some point (perhaps on Radio Pandas??) to let us know more about the intricacies of this research vs. hers.

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I read this. I cannot understand how using the same subjects for 'new' testing is somehow novel or advancing research. He needs to be called out on this.

Actually - this is exactly what happened with Swedo and Cunningham. My understanding is that the blood from the PANDAS group in Cunningham's groundbreaking work came from the first 50 kids from Swedo's 1998 study.

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I haven't read the entire article just the abstract, and as I recall Cunningham herself and her last paper did disclose that her findings did not correlate with previous findings in regards to D2 (I think?). It's your most recent paper and she talks more about the ratio of D1 to D2.


He doesn't mention can kinase II or anti-lysoganglioside or D1, and his testing group is very small. There could be a great many anti-neuronal antibodies that are not tested for, which is why I think Dr. Cunningham uses the cam kinase more heavily than the specific anti-neuronal targets.


It would be interesting to see a comparison for syndenham chorea subjects that have had complete recovery, versus those that have refractory(treatment resistant) OCD- which I believe about 20% have according to an old research article I read.

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He doesn't mention can kinase II or anti-lysoganglioside or D1, and his testing group is very small. There could be a great many anti-neuronal antibodies that are not tested for, which is why I think Dr. Cunningham uses the cam kinase more heavily than the specific anti-neuronal targets.


It is interesting that he did not explore this aspect. I want to believe there was a scientific reason for this, but I find myself wondering if it either was explored and did not come out in a way that Singer wanted, so it wasn't published, or if it was not explored because the likelihood of tipping the scales in favor of the PANDAS hypothesis would be too high.

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He may not have the lab to do it like Dr Cunningham does.


Dr Singer is a Tourette's expert at Johns Hopkins. My personal belief is he, the great expert, missed PANDAS, because surely there were PANDAS kids amongst his Tourette's kids. Someone else came along and embarrassed him. Now he must show the world he was right and everyone else is wrong. Ego.

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