Rick, too much harmony! It makes sense, your explanation. Let me have a cold shower and think about it. I know that you know anecdotal episodes are not good enough for science. However time is running out, so maybe I shall give supplementary a new chance. This time with goodies from NOVARTIS or GLAXO.
Aleks

I'll also add that rifampicin (different class of antibiotics) has been shown in vitro and in vivo (mice) to stop alpha-synuclien aggregation - see below. It is actually planned for phase II studies for MSA - a similar disease. While the mechanism is proposed more than just an anti-inflammatory response - I am sure that helps.

I think that just like everyone has their own story as to genetic susceptibility and triggering event - everyone responds differently to anti-inflammatories/immune modulators. Some people may respond better to antibiotics, herbs (curcumin, EGCG, skullcap/baicalein, etc), low-dose naltrexone, etc. Of course most of these also have properties other than anti-inflammatories so you never know what mechanism is working but its likely the aggregated effect. Thats why I believe (as others do on the forum) you need to support/attack on multiple levels.

Rifampicin inhibits alpha-synuclein fibrillation and disaggregates fibrils; Chem Biol. 2004 Nov;11(11):1513-21.

Rifampicin reduces alpha-synuclein in a transgenic mouse model of multiple system atrophy.
Neuroreport 2008;19(13):1271-6.


Double-Blind, Randomized Trial of Rifampicin on Neurologic and Autonomic Function in MSA

MSA is a uniformly fatal neurodegenerative disease. Evidence from a mouse model mimicking the MSA synucleinopathy suggests that the antibiotic rifampicin inhibits development of aggregates and may disaggregate them. We propose a double-blind placebo-controlled clinical trial of rifampicin 600 mg qd x 12 months in 100 subjects with relatively early MSA. The primary endpoint is the UMSARS1 scale.

Hi there,
A long shower it was.
I cannot help uttering a tiny piece of advice: don’t equate inflammation with infection! They are not the same. Many of you know this, but probably not all of you, so I venture saying this, because it’s such a common mistake. Infection denotes invasion by microorganisms, like bacteria or viruses. Inflammation is the body’s response to tissue damage caused by events such as trauma, heat, cold, sunburn, chemicals, autoimmune reactions, and infections. Infection thus constitutes one of many potential causes leading to tissue damage and ensuing inflammation. The causes and mechanisms leading to neurodegenerative disease, like PD, are generally unknown, but inflammation is high on the list of suspected mechanisms. If inflammation does play a role, it is furthermore unknown what precipitates the inflammatory reaction. Antibiotics would only help if it the cause is bacterial infection. To my knowledge there is no evidence of ongoing bacterial infections in our PD brains. If it had only been that simple!
What about rifampicin and MSA? Rifampicin, or related compounds, may turn out to have beneficial effects on some kinds of neurodegenerative diseases, but don’t yet think of this as the solution we are waiting for. Rifampicin is an antibiotic, and does seem to inhibit protein aggregates in the brains of transgenic mice overexpressing human alpha-synuclein (an experimental animal model for MSA). However, MSA is not PD. Mice are not humans. Transgenic mice are not normal mice. Most important, the mechanism behind the effect of rifampicin on the mouse model is possible related to antioxidant effects, and in all probability unrelated to its antibacterial effects. Furthermore, the group behind the transgenic mice study suggests a clinical trial study on human MSA patients. As far I can see, there are no results from such a study. Finally, rifampicin is far from an innocent drug, with liver toxicity as one of several side effects. There may indeed be something about trying to reduce inflammation, but not by fighting non-existing bacteria with antibiotics with all kinds of side-effects.
It is important to keep up hoping for cures, in our lifetimes, so I’m sorry if I have spoilt a certain kind of beautiful hopes with ugly facts.
Aleks
Heavy this, is this the standard on Neurotalk? I have to use what is left of my precious brain

I think everyone appreciates posters sharing what they think. I for one don't need things sugar-coated, and the plainer we post the easier for everyone to understand.

We have had many posts that I remember where someone has posted something extremely optimistic, and others have posted in response to be cautious. This does not mean we should not be optimistic, we just need to be realistic as well. It is easy to seize onto something and think "this is IT!" because we are so desperate, but thankfully we have many brilliant minds on here who are able to bring reality back into the picture.

It is also easy to forget things, since we all read so very much about PD, and it is very good to be reminded of things like you did, that not all inflammation begins with an infection, an invasion by a foreign organism. So I thank you for your post, and hope that you will continue to share your thoughts and insights.

I could not agree more. The problem is that many people are desperate. It is a horrible disease, no doubt about that. Inflammation might very well be an important actor in this diabolic thing called PD. The conclusion drawn about causality is not plausible, my opinion.
Aleks

I told you NT was different.

Hi Aleks,
thanks for you really great post, it is very illuminating and wonderfully clear.

It raised more questions though, that perhaps you may be able to answer.

While i can see that there is a separation between inflammation and infection, and that there is no direct causality known between PD and infection, I wonder if you could comment and maybe clarify some things about infection.

In MS for instance which as I understand it, is both autoimmune and neurodegenerative, there seems to be an acknowledged link between infection and worsening of MS symptoms, or initiating a relapse.

I have seen many posts over the years that relate to infection and PD symptoms worsening, and the taking of antibiotics improving PD symptoms.

Is there a medical view on why this would happen, other than a general dip in health? I have also seen posts where the opposite is happening, maybe a general infection like a cold, and PD improves. I've observed that the deterioration described, anecdotally of course, often related to bacterial infection, and the improvement related to viral........ it has struck me as interesting, and perhaps significant, and certainly matches my own experience, a cold or flu will knock me sideways in a wholly expected way, but something like a UTI or a dental infection will worsen everything.

This seems very similar to what happens in MS.......

I would love to know what your thoughts are on this. Sometimes I think we are pattern matching because we haven't a clue why things are happening to us, and other times I think that our collective experiences hold truths that have not yet been recognized.

Lindy

Ron's tooth-
" I broke a tooth last week, which got infected, and within 2 days had the most serious relapse I have ever suffered. I had to be helped to dress, helped into bed etc. I literally could not move when unmedicated. My meds did not work, until I increased them to unheard of levels, and visited the dentist. Trouble was I was now writhing around with dyskinesia, and he put a temporary filling in, with disinfectant, and then abhorted the appointment.
In the meantime, my neuro advised me to have it extracted, rather than try to save it, and get totally clear of infection. That is arranged for 2 days time. The inflamed gum has receeded to some extent, presumably due to the disinfectant in the filling, and I am improving.
I did not realise an infection could cause such a trough in symptoms, so thought it worth posting, in case others are also unaware. I did a search and found plenty of evidence for the link between infection and a relapse in symptoms. See

http://goliath.ecnext.com/coms2/summ...99-6764595_ITM
Infections, drug changes can bring Parkinson's to the ED.(emergency department)

http://www.foxnews.com/story/0,2933,146096,00.html
There are a lot of different processes that can make Parkinson's worse, and infections are one of them."

Anyone else had a similar experience? Seems we have got to beware
gum infections, skin infections, measles, urine infections, herpes, gut infections etc.
Ron
__________________
Diagnosed Nov 1991.
Born 1936 "

From there it jumps to http://neurotalk.psychcentral.com/sh...infected+tooth

....before Ron gets back and finds that his BBB thread was thoroughly hijacked in his absence.

,,, , , I have had surgery for a toxic goiter years ago and have 1/3 of my thyroid left and take 0.150 synthroid daily), and I have been diagnosed as having Sjogren's, and fibromyalgia? I believe my autonomic system comes to play in these neruroinflammatory situations. I am also having lots of dental work done, and due to recent foot surgery must take antibiotics, another inflammatory situation in close proximity of my brain.

Rick, I believe you are correct (enen though I don't completely understand all that you said).
Peg