Too funny!

This reminds me of a story my dad tells about how his car was run over by a horse when he was a teenager ...........

Just moved into an apartment with QUIET HOURS. which reminds me: bedding down on Paula's floor on an air mattress a few years ago, Paula peering over the edge of the daybed and challenging me to get up feom the billowing floor, our howling laughter was interrupted by her daughter's emerging from the bedroom and sternly scolding us for waking the baby!! The role reversal was too much for us, and we howled the more.

I dunno, pals, 3000 miles in July-early August was enough for me. Maybe we could meet at Walmart.

Go, Paula!

Jaye

Welcome to the Left Coast, Jaye - it took you long enough!

I hear Walmart is THE place to be!

http://www.ryanseacrest.com/blog/wha...medium=twitter

I'm rather sick at the thought that MJFF had a research roundtable here in Portland, only about a week before we got here, and I had received an invitation in my email!

blue, of course it is. The minute an observant patrician like Bob Dawson recommends a place, well, that's where all yearn to be!

Debi, if you survive this thread, come back to Portland soon!

Jaye

Blue Dahlia - LMAO! That lady must be a babyboomer or the parent of one.

Jaye, I'll come to your Walmart, you've already seen mine.

paula

Paula asked,

They are saying we have "cholinergic dysfunction" and "acetylcholine deficits." early on in the disease. They also say : " the disorder does not become worse over time in PD patients without dementia, as it does in Alzheimer disease (AD)."

They are saying that acetylcholine deficits are evident in diagnosed pd patients who have yet to be treated and this could be a biomarker. Does that mean they are low in acetylchoinesterase or in the actual acetylcholine? Does being low in acetylcholinesterase mean there's not enough acetylcholine to degrade, which is its job?
Paula said that.

Bob said:
Anybody who knows the vocabulary of the research inside out and can explain it to us in straight talk, here's an opportunity to counter-act some of the bafflegab that swirls around in the wind. Lots of very experienced people on this site; experienced in Parkinson's. Just wondering whassup about this thing. Straight-talk, open talk, among people who really do, actually, care a lot about eradicating this Beast from the face of the earth, forever. Maybe it takes generations to achieve, we don't know. But we do know it will require some exchanges of information and opinion and hope and fear such as we find on this site, and it would be good when we run into a big "whassup" that some kind of science people try to translate to us what the situation is. And over time they will find that they learn a lot from the critters on this site.
I am not singing "We are the world". I am writing graffiti that says, "Parkinson's is the last 10% of those brain cells. What killed the other 90%? The 90% that died before Parkinson's. What was that disease called?"

But Paula's question is the one that we lie awake looking at. Someday, one of these things will lead to a cure. This one? The next one? Helps if sometimes we get inside info about what condition our condition is in. Can anybody help us figure out what Paula is on to here?

bob, i appreciate your encouragement and have become engrossed in PubMed trying to see if there is a way to connect the dots between acetylcholine, immune system, and inflammation and are the connnections significant.

I was going to start a new thread on this since we did actually have fun in this one. but i'll try the first one here and then maybe change it to its own thread. It is vastly understudied and some offer reasons why you should reduce acetylcholine... others point out it's importance and imply we shouldn't mess with it. Maybe we will become deficient someday, but are young onset deficient? The biomarker study is the perfect opportunity to measure transmitters. They probably are already .
First it's time to learn abbreviations. Acetylcholine is ACh, mAChR is the muscarine ACh receptor, nAChR is the nicotine ACh receptor. AChE is acetylcholinesterase , the enzyme that breaks ACh down.

I have collected articles that for one reason say we need to lower our acetylcholine and articles that say it is important to have enough because it reduces inflammation.

But not all ACh transmissions are neurotransmissions . Acetylcholine connections are thruout the body and do affect the immune system and inflammation thru the Vagus nerve. i have also found an article describing acetylcholine involvement in apoptosis.

so results are all over the map. debi will probably respond saying they financed all the studies i'm finding in the later 2000s . that would be cool
keep going. i say....i'd be surprised if there is no connection to pd and i am a believer that PD is an immune disorder. The initial insult might be something environmental or increasingly is looking to be genetic.

a last question for this post . do studies keep good, permanent stats on ages of the people. That would be a database in itself. just being able to access how many people, how llong they've had it, age of onset, and age when getting this PET scan.

for starters:
don't see date and it could be older but it has lots of info once you figure out the yin yang qi, etc associations. it makes connections - cause and effect.

http://www.pacificcollege.edu/pcom_s...f/JFratkin.pdf

I can see it now . . . in our section of the country they call it "Fellowship Tours" where the group of travelers have a mean age of 70 years old. They travel all over the place staying in homes of the Amish or in the refurbished traincars of yesteryear. For some reason, however, I don't think a group of young-onset parkie pill-poppers would be so widely accepted by the uninformed public, but opening our own individual homes might be nice (IF ANYONE DARES!) lol

Paula, you remember Chy's "Travels With Parkinson's?" The concept was ingenious. Chy traveled all over the place to PD events where he set up his radio show (free streamlining via the internet). In advance he would set up interviewss or would just talk with people attending the event. It was really informative. And yes, it would likewise make a good fund-raiser.

Let's talk more about it here. Ideas of how to initiate? You almost have to have a non-profit status or go through an established one. You will just get nickel and dimed to death without donors being given a tax break.

Lots to talk about
Peg

Okay...well I have certainly missed some action. I won't try to jump in on all elements of this post but can try to illuminate some of the science around ACH (with some help from Todd Sherer).

Among it's multiple functions in the brain, ACH is involved in motor and cognitive activities. Given these two functions, what do we know about involvement of ACH in PD? And how is it being used as a treatment?

Anti-cholinergics have been used as symptomatic motor treatments (in fact they are the oldest medicines used in PD albeit perhaps not often). In the case of motor treatments, the drugs are blocking ACH. For cognition, the goal is to increase ACH. This based on evidence from AD that there is a reduction in ACH (and we see the same in PD). Today, Exelon is used to treat dementia in PD (originally it was used for AD and later LBD and now PDD).

In terms of biomarkers...there have been studies to measure levels of ACH in the brains of PD patients and relating it to motor and cognitive function http://michaeljfox.org/research_MJFF...s_3.cfm?ID=186. Measures of ACH have not been included in the PPMI study at this time. Basically because the available data seems more relevant for mid and later stage patients (and PPMI is looking in newly diagnosed patients where the balance and gait and cognitive decline symptoms referenced are less frequently observed). Perhaps if we follow the cohort for a longer period or add a mid- late stage cohort. Remember, PPMI is looking for robust markers of progression in early disease. ACH imaging would add significantly to the patient burden and didn't make the cut given other priority imaging needs/opportunities (DaTscan and structural and DTI MRI).

Hope this helps,

Debi