I was curious about the acetylcholine connection too, Paula. I have searched all over Pub Med, but I think the cholinesterase inhibitors like Aricept are quite different than CDP choline.

With drugs like Aricept, an inhibitor prevents the breakdown of Acetylcholine in our brains (key for AD patients but maybe not so key for us). We then end up with more of an imbalance between Acetylcholine and Dopamine. With CDP choline, it is more of a synthesizer, a precursor to Acetylcholine (much like levodopa is to Dopamine), so I don't see that it may result in more but rather naturally enhances production of what we already have. I looked on PubMed and the Web; it seems that Choline's primary role in neurotransmission is to stimulate receptors, much like the agonists do. The key is it works on both Dopamine and Acetylcholine transmission, so it actually may work more to keep things in balance. At least this is what I glean from the research...mind you I got a C in chemistry.

What leaps out at me are the citations in PubMed that show in animal models increases in dopamine receptor density and increases in brain synapses. This is huge! Also, I think it inhibits the inflammatory toxic whirlwind in our brains- not sure on this last one but thought Rick posted something on that one, but I could be mistaken.

I am desperately trying to get my Sinemet intake under control, and it has shown to cut down levodopa dosages by half. I will; however, proceed with caution. We do need to remember that we are playing with an already unlevel playing field of neurotransmitters, so thank you for the word of caution.

Laura