[Conductor71]

Hmmm...I noticed after taking Chinese Skullcap today (along with a few other anti-inflammatory herbals) that I was off the charts with the dyskinesia today. I swear I've lost at least three pounds in water weight since 8:30 am this morning! I was reading the new post on its anti-inflammatory qualities and noting how well it seems be working with a wayward tooth thhat started causing pain. Pain is gone and I have too much dopamine all of a sudden... I've hit the PWP lottery

I started looking into how Skullcap interacts with our neurotransmitters when it just hit me...all of the anti-inflammatory herbals discussed here lately are also MAO inhibitors that prevent dopamine reuptake and leave our brains with a little more to go on. I find this interesting that the herbals ease the chronic inflammation, show neuroprotective properties, and all are MAO Inhibitors?
This is why TEVA is pushing the Azilect studies on neuroprotection. So this is something you probably have discussed or some here may already have the answer? How is it that MAO inhibition is neuroprotective? In other words, by inhibiting it, do we naturally stimulate or enhance neurons we have left? Grow more? I am sure this has to be covered somewhere....

Laura

[olsen]

from an earlier posting:
(MB Youdim, MD, one of the principal developers of Azilect, maintained inhibiting just MAO-B doesnot stop the breakdown of dopamine; that MAO-A is also necessarry in conjunction with MAO-B for that to occur. He stated at the WPC in 2006 that azilect works by regulating the apoptotic pathway in the mitochondria and also prevented opening of the permeability transport pores of the mitochondrial membrane. the following is from 2003, when the data did not support neuroprotection from azilect...we are hopeful it is neuroprotective since my husband takes 1mgm/day.

http://www.rasagiline.com/propargylamines.html

Anti-apoptotic function of propargylamine
inhibitors of type-B monoamine oxidase
by
Naoi M, Maruyama W, Youdim MB, Yu P, Boulton AA.
Department of Brain Sciences,
Institute of Applied Biochemistry,
Yagi Memorial Park, Mitake, Kani-gun,
Gifu 505-0116, Japan.
Inflammopharmacology. 2003;11(2):175-81.

ABSTRACT
In Parkinson's disease and other neurodegenerative diseases, (_)deprenyl, an inhibitor of type B monoamine oxidase (MAO-B), has been proposed to protect or rescue declining neurons. However, clinical trials failed to confirm the neuroprotection, even though in vivo and in vitro studies suggested the possibilities. This paper describes the activities of propargylamine MAO-B inhibitors against apoptosis induced by an endogenous selective dopaminergic neurotoxin, N-methyl(R)salsolinol, in dopaminergic SH-SY5Y cells. A series of propargylamines were shown to suppress the apoptotic cascade; preventing collapse of mitochondrial membrane potential, activation of caspase 3 and fragmentation of nucleosomal DNA. Among propargylamines, (R)-N-propargyl-1-aminoindan (rasagiline) was the most potent at preventing cell death. Rasagiline also prevented opening of permeability transition pore in insolated mitochondria. These results suggest that rasagiline and other propargylamines may regulate the apoptotic machinery in mitochondria and rescue or protect deteriorated neurons in neurodegenerative disorders.