First of all, how could it not be? Second, the antibodies were found in older PWP but not younger?? Twenty years ago....


1. Zh Nevrol Psikhiatr Im S S Korsakova. 1993;93(6):7-11.

[Dopamine antibodies in parkinsonism patients and their possible role in the
pathogenesis of the parkinsonian syndrome].

[Article in Russian]

Man'kovskiĭ NB, Karaban' IN, Kryzhanovskiĭ GN, Evseev VA, Magaeva SV, Vetrila LA,
Trekova NA, Basharova LA, Golubev KM.

Dopamine antibodies (DAb) were found in the blood serum of parkinsonian patients,
middle-aged and elderly, but not young. There was a correlation between the DAb
incidence and dominant symptom in the middle-aged and elderly patients and
between DAb and anginal parkinsonism in the elderly patients. DAb-binding serum
gamma-globulins of parkinsonian patients injected into rat caudate nuclei induced
the pathogenetic mechanism of Parkinson's syndrome (the generator of
pathologically enhanced excitation-GPEE) in this brain part and evoked main
parkinsonian symptoms (oligokinesia, rigidity and tremor). This effect was more
expressed in the elderly rats compared with the young animals. The DAb role in
the Parkinson's syndrome pathogenesis and in L-DOPA therapeutic tolerance
formation is discussed.


PMID: 7512781 [PubMed - indexed for MEDLINE]

that the older you are, the more antibodies you might have. Twenty years ago was the beginning of the agonists coming out on the market wasn't it? How many older patients even had a choice then?

We all feel that there is an auto-immune factor going on and it is important. Just not enough alternatives. It also may suggest that we are talking different syndromes.

Medicines can stop your normal production of a substance. It's a matter of how much you need to function. There certainly are not enough choices.

Furthermore, they are finding that people have anti basal ganglia antibodies (whatever that means- is it an umbrella for dopa and other key neurotransimitters in this area of brain) post streptococcal infections. These infections are now commonly connected to behavioral changes and movement disorders in children known as PANDAS. The most common is sudden onset OCD. If caught early enough, it is treatable and reversible. They are also now noting cases of similar things in adults; the behavioral component isn't as intense or obvious. Happened fairly recently in England in 20 or so people - strep inection resulted in a lethargica type illness onto Parkinsonsism some went on to Parkinson disease. In all these cases, ALL patients have anti-basal ganglia antibodies.

There has long been evidence that PD etiology involves our humoral immune system; massaging the b and t cells of this system is at the core of the new vaccine being developed by Gendelmann at U Nebraska. If this doesn't tell us we have an auto-immune disorder...I give up. My next question is why did it take so bloody long for them to figure that out? It seems to me one of the first things you study and eliminated before you diffuse all research efforts. Just common sense.

My question as this looks increasingly autoimmune, why are we not as a default tested for or screened for anti-bodies? Or at least worked up to see if we seemed to be fighting low level infection. If this had ever been done systematically, we could be years ahead in research and better treatments. There really needs to be some drastic changes in transferring from the lab to the clinic. I will be a guinea pig; sign me up.

Anyway, have citations but on way out the door. Will add later.

Laura

This discussion brings up the inflammation of the brain issue being part of Parkinson’s epidemiology. I believe soome of us a re genetically predispositioned to not be able to tolerat normall inflammation introduced iinto oour bodies (thus, the autoimmune topic). I have adhered to that theory since I first read it in this forum. If I get a cold, a sinus flare-up, or an injury or infection anywhere in my body, my symptoms exacerbate. Does that happen to any of you?

I had to post some of these studies that keep pointing to gene therapy being the wave of the future. (Note the DBS-resistant” reference)

Hmmmm . . . I wonder what “levodopa/STN DBS-resistant axial features” look like?

The 202A deletion of the parkin gene causes early-onset Parkinson's disease with marked levodopa/STN-DBS-resistant axial features. Postural tremor and preserved cognition, even after 40 years of disease, were also evident
Mov Disord. 2011 Mar;26(4):719-722. doi: 10.1002/mds.23456. Epub 2011 Jan 21.

This is a much older study but has a good explanation of the mutations (not deletions)of genes in different phenotypes in PWP’s:

Mutations in the parkin gene are therefore not invariably associated with early onset parkinsonism. In many patients, the phenotype is indistinguishable from that of idiopathic PD. This study has shown that a wide variety of different mutations in the parkin gene are a common cause of autosomal recessive parkinsonism in Europe and that different types of point mutations seem to be more frequently responsible for the disease phenotype than are deletions
Hum Mol Genet. 1999 Apr;8(4):567-74

The need for MORE assessments using non-motor symptoms is great. This recently published (not even in printed hard copy yet) establishes this needed change in outcome measurements.

Arousal symptoms (Epworth sleepiness scale and sleep/fatigue domain of the nonmotor symptoms scale for Parkinson's disease) and pupillary unrest were assessed in 31 participants (14 patients with Parkinson's disease, 17 controls.

RESULTS:
Participants with Parkinson's disease reported more arousal symptoms than controls. Pupillary unrest, arousal symptoms, and Unified Parkinson Disease Rating Scale Part III were positively correlated. The association between nonmotor symptoms scale-sleep score and pupillary unrest was higher in participants with Parkinson's disease than controls and higher in those with more Parkinsonian motor signs. Unified Parkinson Disease Rating Scale Part III was positively associated with pupillary unrest.
CONCLUSIONS:
Pupillary unrest correlates with motor and nonmotor features associated with Lewy-related pathology, suggesting it may be a nonmotor marker of progression in Parkinson's disease

Mov Disord. 2011 Apr 19. doi: 10.1002/mds.23628.

I very much appreciate seeing researchers attempt to find new ways to measure study outcomes, especially when there is no guarantee that those participating in a study have – REALLY have – idiopathic Parkinson’s to start with!
Peggy

Peg-
Go to my blog (see below) and read up on neuroinflammation. It isn't your imagination. An infection anywhere outside the BBB can and does trigger neuroinflammation within the BBB. Remember Ron's abscessed tooth and how bad his PD got?