Parkinson's Disease Tulip


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Old 12-24-2008, 05:00 PM #11
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Default infectious origin of diseases

Husband developed shingles ~3 yrs prior to PD diagnosis and ~2 yrs prior to first physical symptoms of PD.
Think I have mentioned an evolutionary biologist, Paul Ewald, before. an introductory article appeared in the Atlantic Monthly in 1999. Part I, II and III of the article:
http://www.theatlantic.com/issues/99feb/germs.htm

http://www.theatlantic.com/issues/99feb/germ2.htm

http://www.theatlantic.com/issues/99feb/germ3.htm

He maintains diseases that occur in a siginficant % of the population (?>1% -i cannot remember the correct #) are all infectious in origin, and that history of determining etiologies of diseases bears him out. I find his writings fascinating and heard him speak ~4 yrs ago to a group of oncologists. At this lecture, he emphasized that HPV is associated with cervical cancer; H pylori with gastric carcinoma; hepatitis B associated with 50% of cases of primary liver cancer ; EBV (epstein barr virus)which causes lymphomas and nasopharyngeal carcinoma, and noted several other infectious agents being studied for their association to other diseases: ie C pneumoniae and atherosclerosis, among others.
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Old 12-24-2008, 09:51 PM #12
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Hi,
Thanks for starting a good discussion. As Olsen pointed out several disorders are due to or atleast associated with pathogens, including viruses and bacteria. Atherosclerosis is the most recent disorder to that list. Pathogens such as CMV, Chlymedia, Pneumococci and several oral pathogens seem to contribute to atherosclerosis. Similarly a group of pathogens could contribute to PD. At this point, we donot have enough data for this hypothesis. If I were to imagine how this process goes, this is one way:

Any single virus or bacteria alone may not cause PD, but if one is prone to PD, there are a couple of ways pathogens enhance that. Two sets of reactions (at minimum) are going on simultaneously within the body contributing to PD. here is the sequence of events

Exposure to pesticides or some other genetic factor triggers PD

person also gets infected with virus x: infection-induced chronic inflammation, toxins released weaken BBB. Inflammatory cytokines and toxins enter brain and cell death amplified.

Many pathogens specially viruses have proteins that are similar to human proteins. For example virus X has a protein similar to a human neuronal protein. person gets infected with virus x
Body generates immune responses to virusX, makes antibodies, but the antibodies can attack both virus and neurons

Patients' BBB is already compromised due to infections. Antibodies, immune cells go into brain and start killing self cells.

What evidence do I have for this hypothesis?
Pesticides and genetic alterations in PD is established.

Infections and PD connection is there, established????

Leaky BBB adn PD: dont know

Ibuprofin treatment which controls inflammmation was reported to slow down PD. anti 0xidants do the same

Amantadine which was originally discovered as anti-viral drug works for PD

Recent paper by a French group shows (in mice) that if immune cells (T cells) are deleted, PD progression becomes slow whih means no auto immune responses and hence no cell death.

Stem cell transplants in animals helped to relieve symptoms for a short period of time, animals were not cured. experimental reports suggested that transplanted cells either died or didnot function. This to me means body is making auto immune responses and killing or silencing transplanted cells.

This whole thing can be tested relatively easily.

Now coming to your question: There are blood tests checking for antibodies as well as pathogen DNA to figure out whihc of the known pathogens are associated with PD.

General inflammation and responses to infection can be measured.

various lab techniques are needed to figure out if PD is auto immune

identifying the pathogen involved in PD will require efforts similar to whats been going on with HIV research

If really a virus is invovled in PD.........treatment for PD will be the same as HIV and AIDS.

Any comments or suggestions?
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Old 12-24-2008, 10:12 PM #13
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Default fungus

Although I haven't had it in awhile, I've had a recurring fungus for probably 30 years. It's round and resembles ringworm in appearance but isn't. I don't treat it anymore, it goes away on its own. Doctor said it involves the immune system. Is this another factor? Anyone else have fungi?

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Old 12-24-2008, 10:19 PM #14
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I've been reading all these recent discussions with much interest. This and the BBB discussions are of interest to me because of family connections with a Tic disorder, Sydenham's Chorea, Autism spectrum. (and the hypothesis of PANDAS - Paediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococci).

I don't want to butt in on your thread but remember there's also Sydenham's Chorea (once known as St Vitus' Dance) which is a movement disorder associated with Rheumatic Fever.

http://www.nlm.nih.gov/medlineplus/e...cle/001358.htm

http://www.wemove.org/syd/syd.html

Quote:
Acute rheumatic fever (ARF) is a delayed inflammatory reaction in response to a streptococcal bacterial infection (i.e., with group A beta-hemolytic streptococci).
Quote:
The specific underlying mechanism(s) responsible for development of ARF remain unknown. However, evidence suggests that the disorder may result from an abnormal immune reaction in which antibodies produced in response to the invading bacterium act against certain of the body's own cells.
http://www.wemove.org/syd/syd_sym.html

Quote:
Sydenham's chorea is considered a neurological complication following infection with particular strains of streptococci (i.e., group A beta-hemolytic streptococci). The initial illness is usually characterized by a sore throat (pharyngitis) that may be followed, within approximately 1 to 5 weeks, by the sudden (acute) onset of rheumatic fever. The symptom-free period between recovery from pharyngitis to the onset of acute rheumatic fever (ARF) is known as the "latent period." ARF is an inflammatory disease (i.e., sequelae) following group
EDITED to add -
This article also mentions PD.

J Neurol Neurosurg Psychiatry. 1995 February; 58(2): 184–191.
ooops, I forgot the link. Here it is.

Journal of Neurology, Neurosurgery, and Psychiatry

Advance information and movement sequencing in Gilles de la Tourette's syndrome.
N Georgiou, J L Bradshaw, J G Phillips, J A Bradshaw, and E Chiu

Quote:
<snipped article> Although the underlying pathogenesis is still speculative, it is concluded that there is much to support the notion that Tourette's syndrome may stem from abnormalities of the major pathways between the basal ganglia and the frontal lobes.
Please note that is a pretty old piece of work but it was one of the articles I'd saved in my bookmarks that mentions both Tourette Syndrome and Parkinson's Disease. Thing is that here we are in almost 2009 and they're still searching for answers.

Last edited by Lara; 12-24-2008 at 10:45 PM. Reason: add link. change wording.
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Old 12-25-2008, 04:39 AM #15
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Book A few comments without reading everything

Paula, I remember talking about that. A neurologist told me that the big pharmas will buy a huge amount of additional space from medical journals, beyond what the journal usually prints. This material consists of articles written by doctors in the pay of the drug company to be a tester for their drug. There's nothing wrong with that, since doctors are needed to do the testing and the money from the pharma helps pay the doctors' salaries so they don't have to leave the academic environment where they're doing research. The articles, though, will tend to be taken with a grain of salt.

At a PAN (Parkinson's Action Network) Public Policy Forum, I forget which one, Story Landis, Director of the National Institute of Neurological Disorders and Stroke (NINDS) since 2003, began her talk by saying that yes, they do talk across disciplines all the time, and yes, they do keep aware of what others are working on. I gathered that there are usually a lot of questions along those lines.

One way of increasing patient-researcher interaction is to participate in research, if possible. The researchers I've worked with have spent a lot of time with me out of sheer gratitude to me for letting myself be tested. I entered the neurological scene a pretty good knowledge of general medical terminology, and I've looked up a lot of words along the way. There is a medical dictionary link at the top of this page.

Our beloved orgs usually have something about the state of the art on their websites, don't they? if not, keeping track of who's doing what ongoing research would be a good job for the orgs, wouldn't it? Barring that, folks could look at the NINDS Funding News at http://www.ninds.nih.gov/funding/nin...2008/index.htm for November, for example, for a glimpse into the future.

I have for many years been receiving the AMEDEO updates in my e-mail. Their subscription procedures are at http://www.Amedeo.com/. It's essentially a clipping service for the disease of your choice. Also see http://www.freemedicaljournals.com/.

There is a PubMed link at the top of this page. I just entered "Parkinson's virus" without the quotes and got a list of 617 articles. Ignoring everything on viral vectors and other nonrelated (to this discussion), at #11 on my search results was:
Quote:
Viral parkinsonism.
Jang H, Boltz DA, Webster RG, Smeyne RJ.
Biochim Biophys Acta. 2008 Aug 12. [Epub ahead of print]
PMID: 18760350 [PubMed - as supplied by publisher
so I clicked on the title and got:
Quote:
Biochim Biophys Acta. 2008 Aug 12. [Epub ahead of print] Links
Viral parkinsonism.

Jang H, Boltz DA, Webster RG, Smeyne RJ.
Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN, USA.

Parkinson's disease is a debilitating neurological disorder that affects 1-2% of the adult population over 55 years of age. For the vast majority of cases, the etiology of this disorder is unknown, although it is generally accepted that there is a genetic susceptibility to any number of environmental agents. One such agent may be viruses. It has been shown that numerous viruses can enter the nervous system, i.e. they are neurotropic, and induce a number of encephalopathies. One of the secondary consequences of these encephalopathies can be parkinsonism, that is both transient as well as permanent. One of the most highlighted and controversial cases of viral parkinsonism is that which followed the 1918 influenza outbreak and the subsequent induction of von Economo's encephalopathy. In this review, we discuss the neurological sequelae of infection by influenza virus as well as that of other viruses known to induce parkinsonism including Coxsackie, Japanese encephalitis B, St. Louis, West Nile and HIV viruses.
Some definitions off the top of my head in my own words:
etiology - the cascade of events that leads to the disease state
encephalopathy - pathology or disease state of the brain
sequelae - conditions that follow as a result of the disease in question.

I can't wait till the article is old enough to appear on the Free Medical Journals site. In the meantime I've got a life to live, and I'm tired from singing in two major festival services last night, on my feet mostly, including rehearsals, for about six hours so I'm off to bed and wishing all a wonderful Christmas or a Teriffic Thursday, you pick.

My point, if I have one, is that there is more openly available information than is generally thought, IMHO.

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Old 12-25-2008, 10:29 AM #16
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While the study below is talking about depression in particular, it makes clear that the potential problems are not limited to the action of a pathogen but also includes our response to its presence. An extreme case is septic shock in which death results not from bacterial action but rather an over reaction on the part of our own systems. In the case of PD, a similar hyper-response by the microglia in the brain kills neurons. In the case of Ron's bad tooth, it wasn't just the toxins flooding his system. There was probably enough "neuroendocrine and neurotransmitter sensitization" involved to kill a lesser man (or at least a less stubborn one )

1: Stress. 2003 Mar;6(1):19-32.

Stress and cytokine-elicited neuroendocrine and neurotransmitter sensitization:
implications for depressive illness.

Hayley S, Merali Z, Anisman H.

Institute of Neuroscience, Carleton University, Canada. shawnhayley@sympatico.ca

Stressful events, by their effects on neurotransmitter and neuroendocrine
processes, are thought to favor the development or exacerbation of depressive
illness. In as much as immunological challenge, may provoke stressor-like
neuroendocrine and central neurochemical changes, the view was offered that
immune activation essentially acts like a stressor and may contribute to the
evolution of affective illness. In this respect, viral and bacterial infections
appear to influence behavioral/metabolic (e.g. fever, anorexia, somnolence) and
neurotransmitter functioning through the release of cytokines, which act as
messengers between the immune system and brain. The present report provides a
brief overview of the neurochemical consequences of proinflammatory cytokine
treatments, particularly the actions of interleukin (IL)-1beta and tumor
necrosis factor-alpha. As well, synergy with psychogenic and neurogenic
stressors are described, as are data showing that cytokines, like stressors, may
have time-dependent proactive (sensitization) effects, so that reexposure to the
treatments greatly augments hypothalamic-pituitary-adrenal activity, as well as
central neurochemical changes. Indeed, the neurotransmitter alterations are not
restricted to hypothalamic nuclei, but occur in several extrahypothalamic sites,
including various limbic regions. It is suggested that by virtue of these
neurochemical changes, cytokines may have both immediate and proactive effects
on mood states.

PMID: 12637204 [PubMed - indexed for MEDLINE]
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Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
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Old 12-26-2008, 02:00 AM #17
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Default Herpes Simplex virus

I mentioned earlier that the only virus I am aware of having is the Herpes virus (cold sores). I asked whether there was anyone else but there was a nil response. However, I did a short search and found it is common in PD to have this virus. For example

http://content.karger.com/ProdukteDB...ame=114785.pdf
"The main finding was a higher herpes simplex complement-fixing antibody level in patients with Parkinson disease than in controls."

However there is a link to brain injury encephalitis,

http://www.sciencedaily.com/releases...0902221735.htm
The most common symptom of infection is a cold sore, but in some individuals the virus can also cause life-threatening inflammation of the brain (encephalitis); 70% of individuals who do not get treatment for this condition die

From the excellent paper Jaye turned up by Jang et al, and the above, viruses are common causes of brain injury. There is a similar connection in Alzheimers. The question I find myself asking is is this true of all viruses or are certain ones more likely to be involved in the etiology of PD.
How do we erradicate them from our system? I did a quick search, but it appears the same as PD, you manage the symptoms but can't erradicate the virus!! A 2008 reference says:

http://www.ahmf.com.au/health_profes...OralHerpes.pdf
"Cold sores are unsightly and uncomfortable and therefore there is great
interest in finding effective remedies. At present, there is no way of eradicating
the latent infection and treatments are directed solely at control of each
outbreak"

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Old 12-26-2008, 08:28 AM #18
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Default virus eradication

I have not read everything posted in this thread yet, but I am wondering why, as Ron pointed out, you can't eradicate the virus that causes cold sores? What damage, if any, is it doing in the body while it sits there, waiting for the next outbreak?

I wonder if eradication has not been found possible by the medical community because they are looking in the wrong place-nutrition. Many have posted about food here before, including the mainstream medical community's woeful lack of education and emphasis on it. We KNOW curcumin gets rid of h pylori, and although that is a "bacteria" and not techinically a "virus", perhaps it is not too far a leap to be able to do the same for PD.

To do that, we would need to know what the virus(es) is/are that causes or contributes to PD, and then find what foods/supplements impact it. Perhaps there are many viruses that are implicated, or only one, and maybe that one virus doesn't even have to be the same from one person to the next to cause PD-ish symptoms...this would explain the variation in symptoms from person to person.

Let me see what my research attempts can turn up. I've got little kids, so this could take some time, but I'm on it.
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Old 12-26-2008, 08:32 AM #19
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Default correction

My post, which I tried to edit but it didn't work, should have read that mainstream medicine is looking in the wrong places and is NOT looking into nutrition as a possible way to cure herpes and other viruses. Geez, I need to learn how to properly use these buttons!
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Old 12-26-2008, 08:51 AM #20
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Default good overview on nutrition and viruses

At first blush, there is tons of info out there about this, but a ton of it relates to AIDS, animals, and then there are all those hackers trying to hack their product. But I did find this, which is a great overview:


"Nutrition, immunity and infection: From basic knowledge of dietary manipulation of immune responses to practical application of ameliorating suffering and improving survival" ...here's the link (Note this quote: "It is now established that nutritional deficiency is commonly associated with impaired immune responses, particularly cell-mediated immunity, phagocyte function, cytokine production, secretory antibody response, antibody affinity, and the complement system (1, 5, 6)."):

http://www.pnas.org/content/93/25/14304.extract
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