Turnip..........as PD affects only 1 in 500 of the population, that might be at too low a frequency to establish itself as a prion mediated disease in those societies in the habit of eating grandad's brain when he passes on........

annebernadette.......my understanding (as a retired molecular biologist with no experience in PD research) is about 5% of PD cases have been linked to mutations in one of six genes. These are referred to as familial PD as their inheritance will predispose to development of disease. The other 95% of cases are idiopathic (meaning of no known cause). There is evidence that idiopathic PD is caused by the naturally occurring alpha synuclein protein misfolding to a toxic form. That toxic form then goes on to damage a structure or biosynthetic pathway in the brain cell causing the cell to die. The familial gene mutations are thought to act by giving rise to damaged proteins involved in the same pathways or structures that toxic alpha synuclein affects.

If black tea acts by slowing down PD progression (and I think that's a very big 'if') then it might affect all forms of PD. If black tea only prevents start of the disease then it probably is only effective against idiopathic PD. The other medicines I've described which are in clinical trials should, if they work, be effective against both types of PD. (More information on those trials from www.clinicaltrials.gov)

three things that seem of particular interest to me
1) why is pd always initially unilateral? the brain is fairly symmetrical and if an infection or toxic protein arrives at one side why not the other?
2) why only the subs. nigra? why are those cells so vulnerable and others resistant?
what is different about them? other cells produce and store dopamine but only these ones are killed off (at least initially).
3) why is it so slow? even prions are faster (unless there is a cjd disaster waiting in the wings). i know many of us believe it has taken 20 or 30 years for our condition to reach this stage. that seems an extraordinarily slow spread.

the reasons i pick the nose (puerile joke) as the main source of infection are
a) the very common loss of sense of smell/taste which often precedes other symptoms
b) the high occurrence of chronic rhinitis in pwp
c) the superhighway between the nose and roughly the area affected by pd which by-passes the blood brain barrier
d) large numbers of alpha-syn in the nose

If I was a mouse with PD
Indeed I should be happy to be
Injected with PGC-1a
If improving my scurry it may

And neither am I a fruit fly
In a student's Laboratoire
I happen to be a human
With a very complex genome

Whilst I wish all the very best
To those who are trying out to test
The cause and the cure of PD
I think I may just stick to black tea

(sorry - may have put this in the wrong place. Too late - I am not doing it again)

Hi Turnip,

I second all your queries. Also from the 23 and me genetic testing I have a slightly increased risk for PD (who knew?!) and the most significant marker amongst the four I have is the one concerned with alpha-synuclein.
As for the suspicion that one has it for a long time I first went to the GP about a change in my balance - nothing much but definite - in my mid thirties, forty years ago.
I have had tendency to a set expression for longer than I care to remember which I have to consciously counteract. My PE teacher commented that I was slow to get going. The list is endless. Like Spike Milligan had written on his gravestone
I told them I was ill. Actually I didn't because these symptoms were so vague but I did harbour the notion that I had a slow growing non-malignant brain tumour which I mostly put down to hypochondria

Whilst I can't begin to understand the complexities of alpha-synuclein and misfolding proteins, the second paragraph of Turnip's message seems to tie in with the latest thinking on the antihistamine drug, latrepiridine. (Or is that too simplistic?)

Since last Thursday i started taking one 200mg Ibuprofen tablet per day. I'm surprised at what a difference its made to my parkinsons symptoms. Even to the extent that yesterday i was able top cut back on my normal intake of sinemet, and without any noticeable impact to my PD symptoms. I know its early days, but for me taking Ibubrofen seems to have really made a difference. Also I'm only taking one 200mg tablet each morning, which is just about the lowest recommended daily dosage.

I would be interested to know if anyone else has tried Ibuprofen or do you have a view on using it?

Regards
bluey

i've been interested in trying ibuprofen but i believe it interferes with my high blood pressure meds so need to get bp down first but exercise is difficult because of pd problems ...

Thank you very much Bartobob for prviding the links re alpha-synuclein. I have been following the links for most of last night and this a.m. ( I had to keep looking up unfamiliar medical terms and of course one link leads to another.) I have learned more about PD and updated my knowledge of biochemistry (such as it was) without dwelling on my PD - if you see what I mean. Whether or not I retain any of it remains to be seen

I think I shall have to give it a rest for a while -my head is spinning. Having just read an article that concludes PD is the result of a faulty fight/flight response ( the susgestion being that the emotional make -up of individuals who develop PD is such that they "freeze" rather than do something more appropriate and this becomes a trace memory) and then to discover that things I have been taught were not good for me (smoking and too much caffiene) may revent the onset of PD, I think a little Mozart is called for.

Despite all the hours I have spent looking at different sites, I have not come across anything that answers Turnips excellent 3 Q's. But I will not give up. I did however find a few articles about the use of some histamines in the treatment of PD, specifically diphenhydramine for dyskinesia and Rivastigine having a significant (+ive) effect on cognitive functions and behavioural problems associated with PD dementia.

Eileenpatricia - some of the articles I read stated as many as 20 years for PD symtoms to be present but not recognised as such. You reminded me of a school report some 40+ years ago which suggested I might approach my work with a little less attentin to detail but with more energy. And it was not a PE report

re Ibuprofen - I am delighted that you find it helpful Blue-eyes. I have read there is a correlation between the use of this and a lower risk of developing PD, but not (yet) that it may reduce the need for levodopa medicines.

From a personal point of view, I will not give this a try. Apparently the reason I am intolerant to PD medication is that my liver does not funtion all that well, possibly due to a childhood illnes, and NSAID's are contraindicated.

Turnip......

1) why is pd always initially unilateral? If PD (along with Alzheimers and Dementia with Lewy Bodies as argued recently (http://211.144.68.84:9998/91keshi/Public/File/41/336-6088/pdf/1511.full.pdf)
is a prion disease then most probably the reason it doesn't start up until late in life is because the cell manages to bin the prion before it reaches sufficiently high concentration to cause trouble. In familial cases the cell manages to identify and dispose of mutant proteins. In the 1 in 500 of us the rubbish disposal system in one of the billions of brain cells gets less efficient as we get older or gets simply overwhemed by toxins, the cell gets unhealthy and alpha synuclein prion form builds up to levels sufficient to infect the neighbouring cells. So in this scenario, PD starts somewhere in the brain and spreads by cell to cell contact. If it is unilateral (do you mean in one hemisphere?)maybe that's because of the geography of the brain's neronal or vascular connections.




2) why only the subs. nigra? why are those cells so vulnerable and others resistant?
Areas of Lewy body inclusions are found elsewhere in the PD brain but the substantia nigra seems particularly susceptible. Some experimental evidence suggests there is more oxidative stress in the subs. nigra due to its high rate of dopamine biosynthesis which facilitates the build up of prion....
(http://www.springerlink.com/content/r6701k82p8462827/)

3) why is it so slow? even prions are faster (unless there is a cjd disaster waiting in the wings). i know many of us believe it has taken 20 or 30 years for our condition to reach this stage. that seems an extraordinarily slow spread.
.....see the answer to 1. PD onset is presumably controlled by the brain's error eradicating mechanisms (autophagy, ubiquitin tagging, apoptosis) but for 1 in 500 of us in one of our billions of brain cells that mechanism falters one day....


Bernadette............loved the poem !