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Old 03-04-2012, 10:25 AM
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reverett123 reverett123 is offline
In Remembrance
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
reverett123 reverett123 is offline
In Remembrance
reverett123's Avatar
 
Join Date: Aug 2006
Posts: 3,772
15 yr Member
Default Why this matters

Since there are several new faces around here who may wonder what is important and what is not, here is the ultra-condensed version-
Microglia are to the brain what white blood cells are to the body. (Brief pause to say that I know that to be a gross generalization but I'm writing for a broad audience. So sue me. ) They are a part of the immune system's first responders who do battle while the rest of the immune system is analyzing the invader to see what specific weapon is on the shelf for this particular villian. Then that more tightly targeted defense is dispatched and the microglia are instructed to put away their blunderbusses to minimize collateral damage. However, some of us were exposed in the womb to byproducts of maternal infections. Others may have encountered the flu as a young adult at just the wrong time. Still others may have an immune system that gets old and grouchy as we do.

The net result in either case is that our microglia are hypervigilant and don't respond to stand down orders very well. For example, in one study where a rat pup was exposed before birth, he received a second exposure for his birthday. It was found that the normal immune response outside the brain was settled and done in a few hours. But within the blood brain barrier the enraqed microglia were still looking for something to kill ten months later. They were not attacking their fellow "me" cells in a true autoimmune reaction, but they still were doing a lot of damage fighting a battle long finished, an autotoxic reaction.

Once this hypervigilant state is set up, a lot of things can set it off. Familiar ones like viruses and bacteria of course. But less obvious ones as well, such as stress and lipopolysaccharide (LPS). LPS is a part of the skeleton left when a bacterium dies. It is so common that it makes up about half the volume of ordinary house dust. We cannot escape exposure. But somethings, such as the plant noted, are able to calm down the microglia and short circuit neuroinflammation. This saves a lot of damage and it also reduces symptoms because the "soup" produced in the unending battle is itself neuroactive and affects our behavior. Thus our interest.
-Rick


Quote:
Originally Posted by Conductor71 View Post
The desert yarrow is ubiquitous in the Middle East and has been harvested by Bedouins for many years to treat a variety of health ailments. It is commonly sold in the region. Incidentally, PD in Arabic people is very, very low.


Anti-neuroinflammatory effects of the extract of Achillea fragrantissima.
Elmann A, Mordechay S, Erlank H, Telerman A, Rindner M, Ofir R.

Abstract
BACKGROUND:
The neuroinflammatory process plays a central role in the initiation and progression of neurodegenerative diseases such as Parkinson's and Alzheimer's diseases, and involves the activation of brain microglial cells. During the neuroinflammatory process, microglial cells release proinflammatory mediators such as cytokines, matrix metalloproteinases (MMP), Reactive oxygen species (ROS) and nitric oxide (NO)...The extract of Achillea fragrantissima (Af), which is a desert plant that has been used for many years in traditional medicine for the treatment of various diseases, was the most efficient extract, and was further studied for additional anti-neuroinflammatory effects in these cells

RESULTS:
We have found that out of the 66 desert plants tested, the extract of Af was the most efficient extract and inhibited ~70% of the NO produced by the LPS-activated microglial cells, without affecting cell viability. In addition, this extract inhibited the LPS - elicited expression of the proinflammatory mediators IL-1β, TNFα, MMP-9, COX-2 and iNOS in these cells.

CONCLUSIONS:
Thus, phytochemicals present in the Af extract could be beneficial in preventing/treating neurodegenerative diseases in which neuroinflammation is part of the pathophysiology..
__________________
Born in 1953, 1st symptoms and misdiagnosed as essential tremor in 1992. Dx with PD in 2000.
Currently (2011) taking 200/50 Sinemet CR 8 times a day + 10/100 Sinemet 3 times a day. Functional 90% of waking day but fragile. Failure at exercise but still trying. Constantly experimenting. Beta blocker and ACE inhibitor at present. Currently (01/2013) taking ldopa/carbadopa 200/50 CR six times a day + 10/100 form 3 times daily. Functional 90% of day. Update 04/2013: L/C 200/50 8x; Beta Blocker; ACE Inhib; Ginger; Turmeric; Creatine; Magnesium; Potassium. Doing well.
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"Thanks for this!" says:
Conductor71 (03-04-2012), GerryW (03-04-2012)