As if this pathway is easily explained by a teacher of learning impaired -young learning impaired -it becomes a cobweb if you get in very far. now the captain is also learning impaired.....we're still afloat tho. enough psychology.
i saw this term today for the first time , or at least the first time i ever focused upon it , remember I am not the scientist, but think my question is reasonable . There is an article from 23and me, which i still owe spit to because my first sample came back. i'll get to it. this will give me the kick in the butt i need because it yields info about pseudocholinesterase deficiency.
Background
Pseudocholinesterase deficiency is an inherited enzyme abnormality that results in abnormally slow metabolic degradation of exogenous cholinester drugs such as succinylcholine. A variety of pathologic conditions, physiologic alterations, and medications also can lower plasma pseudocholinesterase activity.
review: [any good teacher would do so] lol
- cholinergic - vague term that describes the action of the enzyme that breaks down the acetylcholine and keeps it low, as it is supposed to be. when used alone this term can be confusing about whether they are talking about the enzyme breaking it down and keeping acetycholine low, or if the are talking about ....
cholinesterases - when you see the 'esterase' at the end, it means the enzyme that breaks it down
anti cholinesterase - means you are inhibiting the enzyme that breaks down the acetycholine, thus allowing it to accumulate and incease, and hoping to improve cognitive skills in alzhemiers.
pesticide poisoning can attach itself to the cholinesterase enzyme, thus making the acetylcholine higher in people who have been poisoned?? who knows?
23 and me has an article about this and now i'm very motivated about sending in my second sample.
A genetic mutation could affect our cholinesterase enzymes. This sounds to me like something that could actually cause parkinson's in some people. .either genetically or thru poisoning or both.
just to confuse the terminology, this genetic finding is called pseudocholinesterase, which is not the same as anticholinesterase.
Again, PWP may or may not need acetylcholine....if anything they need an anti cholinergic to do the work of cholinesterase.to lower it. it still does not justify giving us yet even more acetylcholine with cholinesterase inhibitors. [aricept, exelon.]
it logically means the opposite does it not? with a genetic mutation, perhaps we have always needed less acetylcholine...our entire lives...starting with cholic, high strung, hyper, excitable. Too much acetylcholine slows or stops the production of dopamine. it paralyzes. our hearts go off beat and even alzheimers patients who need acetycholine end up with pacemakers and heart attack and death.
Could everyone check their results from 23 and me about the gene for pseudo cholinesterase deficiency? And again i could be close but incorrect. please jump in and correct me if my facts or comprehension is off. i can take it and welcome it for the good of all. anti, pseudo, ergic or esterase -yikes
good for pd-
- low acetylcholine [which is normal]-low is good for everyone ..it's excitatory and leads to adrenalin and stress hormone cotisol. must recover from it.
[LIST]working anticholinesterase emzyme to break down acetylcholine
so anti cholinergic drugs do the work of these enzymes, which could be low or damaged by pesticide poisoning that may attach to the cholinesterase inhibitor and make it dysfunctional. if it is dysfunctional and they find a gene i say hip hip hooray. it at least eliminates or identifies another reason for us to have too much acetycholinero
it all comes from ashes and dust, the perfect machine, but we are so far from anyone caring about a real cure. if this topic cannot be answered here, debi it seems worthy of the criteria you are looking for at pdonlineresearch. Can you please have someone begin a thread on this on PDOR?
I'd like to be caught up on the research , maybe they are working on it...but why do they use Alzheimers dementia scales and would they use patients to come up with a pdd scale??
we know lots of incidental and i'm starting to think scientific infor as well- that they miss because for whatever reasons, they don't connect the dots and don't have time to be online to be current.
Would like very much to hear this topic discussed and feel that anticholinergics have room to improve and could truly help us all to relax. at least some of us.
is it any wonder i'm an excitatory mess? many of you may have battles of your own kind, like withdrawal:
[I]changing meds has been elaborated upon by the DA pd drugs halt and withdrawal. it has always been quite difficult to change meds and i never looked forward to it. but my first neuro gave me everything there was before he gave in and prescribed sinemet. i wasn't so unlike you boann i had symptoms for 10 years before taking sinemet.
ok if anyone finds anything about this please join in with what you find. either everyone knows something i don't, or pdd dementia is going to suffer as they will die anyway - we are the ones who have to figure this out, as they will **** you as you watch.
http://emedicine.medscape.com/article/247019-overview