Paula,

I'm trying to come to terms with all these terms too

I understand in a general way how neurotransmission works but needed a visual to fine tune it for me.

I found a really good, clear explanation here with images. http://www.holisticonline.com/Remedi...n/pd_brain.htm

From their site:

In a healthy brain,

During movement, signals pass from the brain's cortex, via reticular formation and spinal cord (pathway A), to muscles, which contract. Other signals pass, by pathway B, to the basal ganglia; these damp the signals in pathway A, reducing muscle tone so that movement is not jerky. Dopamine, a nerve transmitter made in the basal ganglia, is needed for this damping effect. Another transmitter, acetylcholine, inhibits the damping effect.

In Parkinson's disease, degeneration of parts of the basal ganglia causes a lack of dopamine within this part of the brain. The basal ganglia are thus prevented from modifying the nerve pathways that control muscle contraction. As a result, the muscles are overly tense, causing tremor, joint rigidity, and slow movement. Most drug treatments increase the level of dopamine in the brain or oppose the action of acetylcholine.

Paula, I've looked at a few sites, and if I understand this correctly. Due to loss of dopamine we end up with too much acetylcholine and this imbalance leads to the primary symptoms of tremor, rigidity, and bradykinesia. This is why we are prescribed things like Amantadine (anticholigernic) to help modulate this imbalance. See Parkinson's Hope Digest for more info.

An acetylcholinesterase inhibitor like Aricept works to stop an enzyme from breaking down acetylcholine and thus increases their level and function in our brain chemistry. In other words, we already have too much of it to begin with, so our neuros might prescribe Artane or Amantadine, then we are given Aricept which undoes the other two. I just think that given the chaos that ensues when we lose so much dopamine, neuros should be extra careful about messing with the interplay of our remaining neurotransmitters. Especially when it seems like for any given movement we may need more of one neurotransmitter over the other - these drugs are not given sustainably and can't be applied evenly or adjust to what levels are needed from hour to hour. It seems like this could cause even more problems for us, especially given Zucchini Flowers observation with taking Artane.

Not quite sure yet what all this means for dementia. Other than AD = too little acetyl and PD = too much

Hope this helps a little.

Laura