I found this recent article to be very interesting. The focus of the article is on Alzheimer's (in fact it never mentions PD), but what struck me was the possible relevance to PD of much of what was said.

Could pathogen infection really lead to Alzheimer’s?

I've wondered about this myself. But if PD is caused by an infection, why don't we see clusters of PD? Wouldn't people living in the same house, or those treating PWP, the doctors, nurses, caregivers, get it as well?

If PD is caused by a pathogen that isn't infectious in the traditional sense, so it doesn't spread from person to person like a cold, then how does it get in the brain? To test this out, it seems like it would be relatively easy to introduce a pathogen into a mouse brain and see if it lodged in the PD part of the brain. I'm not a scientist, though, so have no idea if that would even be possible.

lurkingforacure said: "... how does it get in the brain?"

Personally, I find the Braak staging hypothesis fairly convincing (i.e. PD starts in the olfactory bulb and the gut wall, and then travels via nerve fibres to the brain stem and beyond).

In this regard I found the following article very interesting. It discusses the case for the "travelling" being done by alpha-syn oligomers and fibrils, rather then by traditional pathogens.

Pathology: The prion principle : Nature : Nature Research

Thanks for your link jeffreyn - it is interesting.

The idea that infectious agents may be significant in some cases of sporadic AD has been round for a while. There is a free-access discussion of this here Can Infections Cause Alzheimer's Disease? | Epidemiologic Reviews | Oxford Academic.

Dr Balin has focused on the possible role of Chlamydia pneumoniae infection in AD.

Some independent investigators have tried and failed to replicate some of his reported findings about this (see article above). It is curious that Dr Balin chose not to mention this in his opinion piece. I can only speculate about the reasons for this omission...

Overall, I would put this concept into the "interesting but unproven" basket - as the authors of the discussion above point out, a lot more work is needed before we know what is going on.

Thanks for your link kiwi33.

You said: "Some independent investigators have tried and failed to replicate some of his reported findings ..."

Yes, but the review article also says that some researchers did report similar results. As their concluding section states: "...studies have shown that certain infectious agents, such as HSV-1 and C. pneumoniae, can induce AD neuropathologic changes in vitro and in vivo."

And as Balin himself says in the interview: "Not enough neuropathologists understand how these types of organisms can promote inflammation and the generation of amyloid and/or tau pathology even though we and many others have demonstrated this experimentally after finding these organisms in human AD brains."

I also note that the review article was accepted for publication in 2012, and that the Balin interview was published in 2017.

Overall though, I would agree that "a lot more work is needed before we know what is going on".

Here is another article on the theme of infection and Alzheimer's disease, but it's focus is quite different from the article with which I started this thread.

Once again though, as I was reading the article I wondered how much of what was said could apply to PD as well.

https://www.nytimes.com/2016/05/26/h...tion.html?_r=1

"Several kinds of infectious organisms may cause this condition.

There is evidence that an Infection by the stomach ulcer bacteria, H.pylori, may play a major role. Certain strains of these bacteria process cholesterol into a neurotoxin almost identical to one found in certain Cycad nuts eaten in Guam that have caused an epidemic of PD there. In mouse experiments it affected primarily older mice. In people the 80% whose bacteria were eradicated showed symptom improvement whereas the 20% who didn't had their condition deteriorate even faster.

There is also some reason to believe that in some cases, if not all, this condition may be due to a different infection, specifically Lyme Disease. Anecdotally, individuals have made amazing recoveries from this condition by being treated for that one.

Here is one case from New ideas about the cause, spread and therapy of Lyme Disease by James Howenstine:

"Larry Powers, a former Mr. America in 1962, became ill with the symptoms of Parkinson's Disease in 1990. Sinemet therapy was taken for eight years but he gradually became worse. He became confined to a wheel chair and required help with eating. After learning that Lyme Disease might be causing his symptoms of PD he started taking TAO free cat's claw (Uncaria tomentosa). Within three weeks he was out of his wheelchair and fishing for 100 pound tarpon."

If the nerve cells are really dead instead of dormant how is this possible? It's like running after a leg amputation. PD is also highly susceptible to the placebo effect so the same question still applies.

As noted, treatment with TAO-free Cat's Claw has rapidly reversed this condition.

This makes sense if it is, in fact, an infection. In one study, 8 out of 8 PD patients were found to have the Borellia (Bb) organism that causes Lyme Disease. Autopsies in Europe of PD patients found the organism in the substantia nigra in all subjects. According to Howenstine: "Dr. Joanne Whitaker relates that nearly every patient with Parkinson's Disease (PD) has tested positive for Bb. Dr. Louis Romero reports that 3 patients with PD are 99% better after TAO-free cat's claw (Uncaria tomentosa) therapy."

Borellia secretes toxins that damage nerves. The low levels of gluathione found in the brains of PD victims might be the remnant of overwhelmed glutathione detoxification. The infection theory might also explain why stem cells planted in the brains of PD patients sometimes also die or go dormant from whatever affected the old brain cells.

Another possible culprit is the yeast fungus causing chronic Candidiasis. Candida yeast polysystemic infection produces acetaldehyde which combines with dopamine to produce salsolinol, a neurotoxin that destroys dopamine producing nerve cells in the substantia nigra.

A type of bacteria called Nocardia asteroides can accumulate in the substantia nigra and destroy cells. Experiments with mice show it capable of bringing on the symptoms of PD.

Some researchers theorize that a strange micro-organism called a Mycoplasma is to blame.

Low cholesterol and milk are also associated statistically with PD. Incidentally, mycoplasma feed on cholesterol.

Cyanobacteria, also known as blue-green algae, is another suspect that has strong neurotoxins. Chief among these is beta-methylamino-L-alanine (BMAA). Cyanobacteria grow in the roots of the cycads in Guam and BMAA is found in the nuts. A study found BMAA in the brains of ALS, Parkinson’s, and Alzheimer’s victims but not in the brains of people who’d died from Huntington’s, a neurodegenerative disease that’s linked to a specific gene. BMAA causes misfolding of proteins leading to Lewy bodies or neurofibril tangles typical of neurodegenerative diseases. It can be found in seafood and certain water sources.

The enteric parasite giardia lamblia produces neurotoxins implicated in PD and other neurological disorders. According to one article, "Giardia also produces neurotoxins—toxins that harm the nervous system. These toxins cause depression, sleep disorders, and an inability to concentrate, among other symptoms. Giardia is linked to autoimmune disease, particularly with neurological autoimmune processes such as multiple sclerosis, ALS (Lou Gehrig’s disease), and Parkinson’s disease."

A recent Chinese study confirmed the role of infections in PD. It concluded, "Infectious burden consisting of CMV, EBV, HSV-1, B. burgdorferi, C. pneumoniae and H. pylori is associated with PD. This study supports the role of infection in the etiology of PD."

If you do a search on this site you'll find that it has been discussed.

GerryW, thanks very much for your substantial post. There are a number of things there which I will look into.

One point I would like to make at this stage is that I think your statement "A recent Chinese study confirmed the role of infections in PD" could be a bit misleading. I read this paper recently and I remember that they do not claim to have established causality. All they claim to have established so far is that "infectious burden" (i.e. the number of different infections you've had during your life) is greater in PWPs compared with non-PWPs. I would agree though, that they have certainly established a relationship between infection and PD.

Perhaps I'm splitting hairs once again!

Many years ago I had very bad Lyme disease with emphasis on meningitis that lasted about a year. I often wonder if that was the precursor to my PD. And I imagine a bad fall from a horse when I was a kid around ten years old didn't help either. But back to my brain and a pathogen, I lost my sense of smell permanently during my Lyme. I am new to this forum. Thanks.