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General : NSAIDS
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 Message 1 of 5 in Discussion 
From: MSN NicknameJamieDH4  (Original Message)Sent: 8/2/2007 6:49 AM
Hans-

I have been trying to find articles on the effects that NSAIDS have on prostaglandin production in the Central Nervous System, but can't seem to find any. Could you direct me to some?

This has nothing to do with my boyfriend taking aspirin, simply for research purposes. I was researching the connection between chronic NSAID usage and reduced risk of Alzheimers Disease, but from what I can see most NSAIDS have poor CNS penetration, so I was wondering how this could be.

any help you could offer would be greatly appreciated.


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 Message 2 of 5 in Discussion 
From: MSN NicknameHansSelyeWasCorrectSent: 8/2/2007 7:56 AM
Did you just try a search engine and use the terms? I found a lot of material, but most was very specific, so I don't know exactly what you are looking for. Is this what you seek:

http://eurosiva.org/Archive/Vienna2005/Speakerabstracts/JCashmanAbstract.htm

If not, there is this abstract:

OBJECTIVE: Neurologic and psychiatric manifestations are severe complications of systemic lupus erythematosus (SLE). As commonly seen in patients, spontaneous development of lupus-like disease in MRL-lpr mice is accompanied by brain atrophy and behavioral dysfunction. We examined inflammatory and ultrastructural aspects of central nervous system (CNS) involvement using a nonselective cyclooxygenase-2 (COX-2) inhibitor and measuring effects on behavior, microglial activation, and neuronal morphology. METHODS: Ibuprofen (IBU) was provided in a rodent chow (375 ppm) for animals 5-19 weeks of age. Exploration of a novel environment and performance in the forced swim test assessed effects on behavior. Immunohistochemistry, fluoro-Jade B (FJB) staining, and flow cytometry were employed in neuropathological analysis. Transmission electron microscopy was used to examine ultrastructural morphology of cortical, hippocampal, hypothalamic, nigral, and cerebellar cells. RESULTS: Chronic IBU treatment failed to normalize immune status, behavior, and brain mass in lupus-prone MRL-lpr mice. It also did not reduce density of CD3+ lymphocytes in the choroid plexus, or FJB+ neurons in the hypothalamus. Activated F4/80+ microglia increased with age, but IBU treatment was not effective in reducing their numbers. Although numerous dark cells were seen in functionally critical brain regions (e.g., paraventricular nucleus and subgranular zone), ultrastructural morphologies of classical apoptosis or necrosis were not detected. CONCLUSION: The COX-dependent pathway does not seem to be critical in the etiology of CNS disease in this model of neuropsychiatric lupus. Reduced brain mass, increased microglial activation, and condensation of cytoplasm point to a metabolic perturbation (e.g., excitotoxic damage) that compromises function and survival of central neurons during lupus-like disease.

Source: J Rheumatol. 2006 Nov;33(11):2199-213.

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 Message 3 of 5 in Discussion 
From: MSN NicknameJamieDH4Sent: 8/4/2007 7:57 AM
Yes, I've tried but I don't think the terms I am searching for are correct because I don't find what I am looking for.

Whether or not it is just a correlation people who take NSAIDS on a regular basis have lower incidences of Parkinson's and Alzheimer's Diseases when taken on a regular basis over 10 year periods.
I don't think either of those could be used to treat the disease, as the abstract you posted demonstrated, but for some reason people who take them more often have lower incidences of those two diseases. I am wondering why it is thought to be the case since those two drugs have poor CNS penetration, or so I am told.

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The number of members that recommended this message. 0 recommendations  Message 4 of 5 in Discussion 
Sent: 8/4/2007 8:10 AM
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 Message 5 of 5 in Discussion 
From: MSN NicknameHansSelyeWasCorrectSent: 8/4/2007 8:10 AM
Well, these "experts" don't seem to think it is unusual:

http://www.healthatoz.com/healthatoz/Atoz/common/standard/transform.jsp?request
URI=/healthatoz/Atoz/dc/caz/neur/park/alert12022003.jsp

On the other hand, there is the usual:

QUOTE: "How inflammation is involved in Parkinson's, we don't know. That's the million dollar question," Chen says.
UNQUOTE.

Obviously, this person does not realize that AA should not be in the cells to begin with, but instead thinks that AA is "essential." Just be glad you are one of the few people who understand this !

:-)

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