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Old 05-09-2011, 09:24 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 This new report sums it up and offers a solution too

As most of you know ad nauseum I have been beating the drum for a combined attack by the immune system causing neuroinflammation further aggravated by stress as the central driver for PD. This short piece in today's Science Daily not only makes the last pieces fit, it offers a promising treatment with a very old, cheap, and (safe) time=tested drug.

"Researchers See a 'Picture' of Threat in the Brain: Work May Lead to New Model of Neuroinflammation

ScienceDaily (May 3, 2011) — A team of researchers is beginning to see exactly what the response to threats looks like in the brain at the cellular and molecular levels.

This new information, including the discovery that a model of social stress can increase inflammation among brain cells, should provide new insight into how the stress response affects inflammatory and behavioral responses.

It may also provide new targets for drugs treatments in the continuing struggle to curtail depression and anxiety.

Scientists from Ohio State University's Institute of Behavioral Medicine Research reported their results in the latest issue of the Journal of Neuroscience....

"These animals can't flee, so they have to stand and fight," Sheridan explained. "In doing so, they're repeatedly defeated, creating a condition called "learned helplessness," a condition closely linked to depression.

What Sheridan and Godbout saw was that the animals' anxiety continued for a long time after the termination of the stressful episodes of defeat. "For two weeks or more after we stopped the stressor, we could still see this anxiety-like behavior," Sheridan said.

The real discoveries came when the researchers analyzed what was happening in the animals' brains and in their immune response.

"We found that in the stressed animals, a certain type of immune cell (myeloid progenitor cell, or MPC), produced in the bone marrow, entered the circulatory system and migrated to the brain," explained Godbout.

These MPCs might normally relocate in this way to deal with an infection or an injury in the brain, but in this case, they moved solely because of the response to a social stressor, he said. The experiments showed that the number of these cells more than tripled in the brain following the stress.

Other immune cells called microglia, normally residing in the brain, also triggered an inflammatory response because of the stress. The researchers also noted that the stressor caused a particular activation pattern of neurons, or nerve cells, within the brain.

The response to social stress also caused an increase in the amounts of some inflammatory cytokines in the brain, including interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-a) which are linked to inflammation. These cytokine responses correlated with an insensitivity of MPCs to glucocorticoids, hormones that normally inhibit inflammation in the body....

So the research team saw these and other cellular changes occurring in the brain following the stress, at the same time they were seeing the behavioral changes -- the anxiety-like behavior.

The findings are evidence of a two-way communication that's existing between the body and the brain in times of stress, Sheridan said.

To test that apparent connection, they gave the mice injections of propranolol -- a so-called "beta-blocker" drug often used for cardiac conditions -- before they encountered the more aggressive mouse. In this case, the researchers saw no increase in IL-1 or TNF-a, no glucocorticoid insensitivity, and no long-lasting anxiety-like behavior in the test animals.

"If we treated the animal with a beta-blocker each night before we put the intruder in, it completely blocked the signal. The anxiety-like behavior never developed," Godbout said.

"What this basically argues is that we may now have a new target for individuals who have extended anxiety-like behavior," Sheridan said. "We may have a new target cell to think about in terms of new therapies...."

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Propranolol is an interesting drug. By coincidence I began taking it about three months ago as part of dealing with the problems that I was having with potassium shifts.
From Wikipedia-
"Propranolol is one of the banned substances in the Olympics, presumably for its use in controlling stage fright and tremors. It was taken by Kim Jong Su, a North Korean pistol shooter who won two medals at the 2008 Olympic Games. He was the first Olympic shooter to be disqualified for drug use.[1]....
"Propranolol is often used by musicians and other performers to prevent stage fright. It has been taken by surgeons to reduce their own innate hand tremors during surgery.[9]

Propranolol 80mg daily should be used post discharge in STEMI patients.

Propranolol is currently being investigated as a potential treatment for post-traumatic stress disorder.[10][11][12] Propranolol works to inhibit the actions of norepinephrine, a neurotransmitter that enhances memory consolidation. Studies have shown that individuals given propranolol immediately after a traumatic experience show less severe symptoms of PTSD compared to their respective control groups that did not receive the drug (Vaiva et al., 2003)....
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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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