[Stitcher]

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

[reverett123]

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