Gentelmen see my latest post:

Parkinson’s disease patients exhibit progressive spreading of aggregated α-synuclein in the nervous system. This slow process follows a specific pattern in an inflamed tissue environment. Recent research suggests that prion-like mechanisms contribute to the propagation of α-synuclein pathology. Little is known about factors that might affect the prion-like behavior of misfolded α-synuclein. In this review, we suggest that neuroinflammation plays an important role. We discuss causes of inflammation in the olfactory bulb and gastrointestinal tract and how this may promote the initial misfolding and aggregation of α-synuclein, which might set in motion events that lead to Parkinson's disease neuropathology. We propose that neuroinflammation promotes the prion-like behavior of α-synuclein and that novel anti-inflammatory therapies targeting this mechanism could slow disease progression.

Badboy, I have read reports where, on autopsy of PWP, they did not find any alpha-synyclein clumps, yet the deceased had been dx'd with PD and been taking PD meds for years.....similarly, there are people who were never dx'd with PD who on autopsy, they found the clumps. Can you reconcile this? To me, all this means is that the clumps are not definitive at all, since some PWP don' t have them (but should) and some non-PD people have them (but shouldn't)!

I have not found any research reconciling these conflicting findings.

Hi Lurking. Do you have any links showing the above results? Thanks.

LURKING, pd is misdiagnosed, essential tremor, vascular pd, are diagnosed as pd. so you'd expect that you'd find some inconsistancies from that angle. not sure about the people with lewy bodies with no pd symptoms. you see the same thing in alzheimers, clumps and beta amyloid but no alzheimers symptoms. you've also have rare mutations that cause young onset pd and maybe mutations that protect neurons even with lewy bodies, just like there are individuals that are immune to aids.. you had the case of those drug addicts who developed a pd like syndrome overnight after taking synthetic heroin which responded to l-dopa, i doubt they had lewy bodies. so there must be different ways to destroy dopamine neurons that doesn't involve alpha syncluien, maybe just just damages other genes? how many different types of breast cancer are there? and how many cancer survivors are there now that the most comnon forms have a cure/treatment yet the uncommon ones are still a mystery? just me making an educated guess, keep in mind we share 1/3 of our genes with broccoli, 99% with chimps, yet look at the diversity.

Hello !

I scanned Dr Paneri's diet and put in Online
All items with X ,are forbidden

cheers

oops here it is :

http://pddiet.blogspot.fr/2014/02/dr...s-disease.html

hello badboy !
what do you mean by adjust ?
you have to increase your dose of nicotine every 2 months by 3,5 mg no more, no less .
don't increase more than 3,5mg every 2 months ,to be effective ,it has to be STEP BY STEP.

kind regards

Hi Villiers! How do I know when I have arrived at my perfect dose. I stopped at 21mg because I'm not sure when to stop? How did you know when to stop? Which symptoms are helped the most in your mind?

...to point these things out And I had no idea we share 1/3 of our genes with broccoli, no wonder I like the stuff so much!

I get that there could be many causes of PD, but don't get why research keeps hammering away on the alpha-synuclein when from everything I have read over the past many years, it is NOT the hallmark it is portrayed to be. I don't have links, sorry, this is my take from cumulative reading over many years.

If someone is dx'd with PD and takes PD drugs for years, but on autopsy, if one is even done, there are no synuclein clumps found----they proclaim no PD. Yet, that person took drugs for that illness for years, suffered, insurance paid for scripts, doc visits, etc....

Maybe by scrutinizing synuclein they will discover what its function(s) is/are, as they don't even know that. Hopefully.

I've been invited to a presentation by Dr. Virginia Lee from the University of Penn, this Friday. She is one of the most renowned authorities in the world on the etiology and pathogenesis of alpha-synuclein, tau, and other misfolded disease proteins in the pathobiology of neurodegenerative diseases. She will be lecturing on the current state of the science regarding misfolded proteins and PD and AD. I will be happy to report back any interesting updates regarding a-syn and PD after the lecture.