,

Hi all,
I posted a follow up question on this topic (what maintains inflammation?) on PDRonline, waiting to hear from PD experts..... I will post my thoughts, some answers to Laura's Q and my Paradigm of PD and immune system my two cents worth!) t0morrow. Inflammation may not trigger PD, but definitely promotes it! More later!

girija

 Inflammation of the CNS is universal among PWP. (Whitton 2007)

 That inflammation can be incredibly destructive and the substantia nigra is particularly vulnerable. (Various)

 At least three paths lead to the inflammatory state. I have labeled them Senior, Adult, and Young Onset.

 Senior is as described by Smeyne, Braak, et al and is initiated by the entry of a pathogen, presumably a virus, though the olfactory and gastric routes into the brain. This triggers the inflammatory immune response which persists long after the pathogen has disappeared. An assumed latency period of twenty years or more would make this population “bunch up” at the elder end of the distribution and account for the “standard” presentation.

 Adult arises from systemic exposure to the bacterial endotoxin lipopolysaccharide (LPS). This could be triggered by either an unusual sensitivity or a particularly egregious exposure. The literature contains a striking example of this in the case history of Ines Niehaus, a young lab tech accidentally exposed to salmonella LPS who developed PD and whose report is available online. Seemingly the latency on this form is highly variable.

 Young onset has a more convoluted etiology and arises from prenatal exposure to the same endotoxin during critical time periods in the development of fetal structures. This form impacts not only the nervous and immune systems, but also the endocrine, particularly the hypothalamus-pituitary-adrenal axis, as shown by Carvey and others. The effect seems to manifest post-puberty. Assuming a 20-year progression to symptoms, this would result in cases becoming evident abou the age of forty. This group is highly influenced by “environmental insult” due to synergistic forces with the LPS.

Here's your question on pdor girija
http://www.pdonlineresearch.org/resp...r-mimicry-work

From the We Move site: Continuing ed course:
http://www.mdvu.org/emove/article.asp?ID=759

"Subject: Parkinson's Disease and Bacterial Infections: Is There a Link? "

"The results of two recent studies support the idea that the loss of dopamine-producing nerve cells may be due, at least in part, to previous bacterial infections. In the first study, researchers found that maternal infection with gram-negative bacteria in pregnant rats resulted in a marked decrease in the number of cells in the substantia nigra in the rat pups that were born. Subsequent exposure to environmental toxins after birth tended to speed up the loss of these cells. In the second study, researchers concluded that an association may exist between a previous infection with a certain bacterium known as Nocardia asteroides and the development of Lewy bodies in people with neurodegenerative disorders. ..."

The work of Evolutionary Biologist, Paul Ewald (now at Univ of Louisville), was profiled in the Atlantic Magazine in 1999 (revolutinary theories in 1999--seems so dated now, though his theories are still around )

Part 1:
"...Genetic traits that may be unfavorable to an organism's survival or reproduction do not persist in the gene pool for very long. Natural selection, by its very definition, weeds them out in short order. By this logic, any inherited disease or trait that has a serious impact on fitness must fade over time, because the genes that spell out that disease or trait will be passed on to fewer and fewer individuals in future generations. Therefore, in considering common illnesses with severe fitness costs, we may presume that they are unlikely to have a genetic cause. If we cannot track them to some hostile environmental element (including lifestyle), Ewald argues, then we must look elsewhere for the explanation. 'When diseases have been present in human populations for many generations and still have a substantial negative impact on people's fitness,' he says, 'they are likely to have infectious causes.'..."


http://www.theatlantic.com/issues/99feb/germs.htm

I take a prescription anti inflammatory every day. I don't know if it is slowing progression, but I believe in it in theory and it actually seems to help symptomatically in a small way. This was at my suggestion, not my neuro's, but he's down wid it.

husband took Mobic, anti inflammatory, for ~ 9 months; developed abnormailties in renal function (as evidenced in renal function testing of plasma). unsure which anti inflammatory you take, and am unaware if this potential adverse effect can occur with the general class of anti inflammatories--just FYI. Obviously, this adverse effect does not occur in everyone who takes Mobic. madelyn

I ran across the following mixture and there are probably others so I'm not going to give a brand on it although if you PM me I will. It makes a good example of what I'm looking for in that the idea of a mixture at low doses where I am familiar with most of the species is good. (Darn, that is a terrible sentence ) Anyway, low dose and familiar names add safety and multiple species allow synergy and cover more bases. If you run across similar mixes I would like to know.

Rosemary (leaf) 100 mg supercritical extract and 50 mg extract (23 % total phenolic antioxidants [TPA]-34.5 mg)
150 mg
*
Turmeric (rhizome) 10 mg supercritical extract (45 % turmerones-4.5 mg) and 100 mg ethanolic extract (7 % curcuminoids-7 mg)
110 mg
*
Ginger (rhizome) 54 mg supercritical extract (30 % pungent compounds-16.2 mg, 8% zingiberene-4.3 mg) and 46 mg ethanolic extract (3 % pungent compounds-1.4 mg)
100 mg
*
Holy Basil (leaf) extract (2 % ursolic acid-2 mg)
100 mg
*
Green Tea (leaf) extract (45 % polyphenols-45 mg)
100 mg
*
Hu Zhang (Polygonum cuspidatum) (root and rhizome) extract (8 % resveratrol-6.4 mg)
80 mg
*
Chinese Goldthread (root) extract (6 % berberine-2.4 mg)
40 mg
*
Barberry (root) extract (6 % berberine-2.4 mg)
40 mg
*
Oregano (leaf) supercritical extract (4 % TPA-1.6 mg)
40 mg
*
Baikal Skullcap (Scutellaria baicalensis) (root) ethanolic extract (17-26 % baicalein complex including baicalein and baicalin-3.4 -5.2 mg, and 0.4-0.9 % wogonin-0.08-0.18 mg)