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04-04-2008, 06:44 PM | #1 | |||
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Magnate
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Begs the questions...Why do I have PD?? LOL
Pieces coming together in Parkinson's, cholesterol puzzle http://www.eurekalert.org/pub_releas...-pct040408.php CHAPEL HILL – In 2006, University of North Carolina at Chapel Hill researchers published a study that found people with low levels of LDL cholesterol are more likely to have Parkinson's disease than people with high LDL levels. But that study could not answer the question of whether low LDL (low-density lipoprotein) levels were present in study participants before they were diagnosed with Parkinson’s, or if they developed low LDL levels after being diagnosed. Now a follow-up study led by UNC researchers in collaboration with colleagues in Virginia, Hawaii and Japan has found that low LDL levels were present in a group of men of Japanese ancestry long before these men were diagnosed with Parkinson’s. “This finding gives us one more piece in the puzzle about the role of cholesterol in Parkinson’s disease,” said Dr. Xuemei Huang, the study’s principal investigator. Huang is also medical director of the Movement Disorder Clinic at UNC Hospitals and an assistant professor of neurology in the UNC School of Medicine. READ entire article
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You're alive. Do something. The directive in life, the moral imperative was so uncomplicated. It could be expressed in single words, not complete sentences. It sounded like this: Look. Listen. Choose. Act. ~~Barbara Hall I long to accomplish a great and noble tasks, but it is my chief duty to accomplish humble tasks as though they were great and noble. The world is moved along, not only by the mighty shoves of its heroes, but also by the aggregate of the tiny pushes of each honest worker. ~~Helen Keller |
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04-05-2008, 03:10 AM | #2 | |||
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In Remembrance
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OK, let me go throught it briefly-
1- Baby is exposed to bacterial toxins (LPS) while in womb 2- Baby's immune system in brain is "primed" to overreact against future LPS exposure 3- Young man has leaky BBB and leaky gut too. LPS makes it to the brain 4- Man's immune cells in brain (microglia) overreact and start pumping out dangerous cytokines which begin to kill neurons 5- A healthy body uses LDL cholesterol to bind and eliminate LPS toxin 6- Low levels of LDL interfere with normal defense : Biochem Biophys Res Commun. 2006 Mar 31;342(1):9-18. Epub 2006 Jan 31. Oxidized low density lipoprotein suppresses lipopolysaccharide-induced inflammatory responses in microglia: oxidative stress acts through control of inflammation. Kim OS, Lee CS, Joe EH, Jou I. Department of Pharmacology, Ajou University School of Medicine, San 5, Wonchen-Dong, Youngtong-Gu, Gyunggi-Do, Suwon 442-721, Republic of Korea. Low density lipoprotein (LDL) is readily oxidized under certain conditions, resulting in the formation of oxidized LDL (oxLDL). Despite numerous in vitro reports that reveal the pathogenic role of oxidative stress, anti-oxidative strategies have underperformed in the clinic. In this study, we examine the role of oxLDL in brain inflammatory responses using cultured rat brain microglia. We demonstrate that oxLDL inhibits lipopolysaccharide (LPS)-induced inflammatory responses in these cells. It also decreases LPS-induced expression of inducible nitric oxide synthase and production of nitric oxide, and reduces LPS-induced secretion of tumor necrosis factor-alpha and monocyte chemoattractant protein-1. Oxysterols, known components of oxLDL and endogenous agonists of liver X receptor, can simulate the inhibitory effects of oxLDL in LPS-activated microglia. In addition, their inhibitory effects were mimicked by liver X receptor (LXR) agonists and potentiated by a retinoid X receptor agonist, suggesting these molecules heterodimerize to function as oxysterol receptors. Taken together, our results demonstrate that oxLDL inhibits LPS-induced inflammatory responses in brain microglia and that these inhibitory effects are mediated by oxysterols and, at least in part, by the nuclear receptor LXR. Our results suggest an additional mechanism of action for oxidative stress that acts indirectly via modulation of inflammatory responses. Although further studies are needed, these results answer in part the question of why anti-oxidative strategies have not been successful in clinical situations. Moreover, as brain inflammation participates in the initiation and progression of several neurodegenerative disorders, the present data provide information that should prove a useful guide for designing therapeutic strategies to combat oxidative brain diseases. PMID: 16466690 [PubMed - indexed for MEDLINE]b
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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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