Quote:
Originally Posted by reverett123
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]
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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