Bang your drum long enough and someone will begin dancing
Some interesting stuff of recent vintage-
For my money this team is the top of the heap: 1: Neurochem Res. 2008 Oct;33(10):2044-53. Epub 2008 Mar 27. Curcumin protects dopaminergic neuron against LPS induced neurotoxicity in primary rat neuron/glia culture. Yang S, Zhang D, Yang Z, Hu X, Qian S, Liu J, Wilson B, Block M, Hong JS. Laboratory of Pharmacology and Chemistry, National Institute of Environmental, Health Sciences, National Institutes of Health, PO Box 12233, Research Triangle Park, NC 27709, USA. Using primary rat mesencephalic neuron-glia cultures as an in vitro model of Parkinson's disease (PD), we tested the effect of curcumin, a natural dietary pigment with well-known anti-inflammation effects, on dopaminergic (DA) degeneration. Curcumin pretreatment mitigated LPS-induced DA neurotoxicity in a concentration-dependent manner and curcumin post-treatment also showed protective effect. Microglia depletion abolished this protective effect of curcumin, indicating that microglia play an important role in this effect. Supportively, observation by immunocytochemistry staining using OX-42 antibody showed that curcumin treatment inhibited LPS-induced morphological change of microglia. Besides, LPS-induced production of many proinflammatory factors and their gene expressions decreased dramatically after curcumin treatment. Results also revealed that curcumin treatment decreased LPS-induced activation of two transcription factors--nuclear factors kappaB (NF-kappaB) and activator protein-1 (AP-1). Taken together, our study implicated that curcumin might be a potential preventive and therapeutic strategy for inflammation-related neurodegenerative diseases. PMID: 18368483 [PubMed - in process] |
Trifolium is a fancy name for red clover
1: Neurosci Res. 2008 Oct;62(2):123-30. Epub 2008 Jul 16.
Protective effect of isoflavones from Trifolium pratense on dopaminergic neurons. Chen HQ, Wang XJ, Jin ZY, Xu XM, Zhao JW, Xie ZJ. State Key Laboratory of Food Science and Technology, Jiangnan University, 1800 Lihu Road, Wuxi, Jiangsu 214122, PR China; School of Food Science and Technology, Jiangnan University, 1800 Lihu Road, Wuxi, Jiangsu 214122, PR China. In the present study, protective effect of five isoflavones (formononetin, daidzein, pratensein, calycosin and irilone) from Trifolium pratense on lipopolysaccharide-induced dopaminergic neurodegeneration was studied for the first time. The results showed that all five isoflavones attenuated LPS-induced decrease in dopamine uptake and the number of dopaminergic neurons in a dose-dependent manner in rat mesencephalic neuron-glia cultures. Moreover, they also significantly inhibited LPS-induced activation of microglia and production of tumor necrosis factor-alpha, nitric oxide and superoxide in mesencephalic neuron-glia cultures and microglia-enriched cultures. In addition, the rank order of protective potency of five isoflavones was: pratensein>daidzein>calycosin>formononetin>irilone . This study suggested that all five isoflavones protected dopaminergic neurons against LPS-induced injury through inhibition of microglia activation and proinflammatory factors generation. PMID: 18675857 [PubMed - in process] |
hypothesis but what the hey...
1: Med Hypotheses. 2008 Aug 19. [Epub ahead of print]
Impact of glucocorticoids and chronic stress on progression of Parkinson's disease. Kibel A, Drenjančević-Perić I. Department of Physiology and Immunology, School of Medicine, University Josip Juraj Strossmayer in Osijek, J. Huttlera 4, 31 000 Osijek, Croatia. Parkinson's disease, a chronic progressive neurodegenerative disorder, has a mainly unknown multifactorial etiology. It is characterized by progressive degeneration of dopaminergic neurons. Chronic stress, a condition mediated by elevated concentrations of glucocorticoids over an extended period of time, has been shown to be unfavourable for neurons and to cause damage and neuronal loss in certain brain areas. Glucocorticoids are most probably not toxic in a direct manner, but can make neuronal damage through several potential indirect mechanisms in combination with other destructive factors. We postulate that chronic stress will have a harmful effect on patients with Parkinson's disease, facilitating neuronal degeneration and accelerating progression of clinical manifestations. The damaging impact on neurons will not be because of direct cytotoxicity, but by putting them into an energetically unfavourable condition, in which they will be more sensitive to destructive factors caused by the primary process. Possible mechanisms include elevation of excitatory amino acid concentration, which are excitotoxic, disruption of calcium homeostasis, metabolic disturbance or impairment of neurogenesis. This could have significant implications for patients with Parkinson's disease and chronic stress, or patients with glucocorticoid treatment for various immunopathological diseases, as well as patients with abnormal secretion of glucocorticoids such as in Cushing's syndrome. If confirmed, this hypothesis would represent a valuable advancement in care of patients with Parkinson's disease. PMID: 18718724 [PubMed - as supplied by publisher] |
and last but not least
1: Brain. 2008 Jul;131(Pt 7):1880-94. Epub 2008 May 26.
Central and systemic IL-1 exacerbates neurodegeneration and motor symptoms in a model of Parkinson's disease. Godoy MC, Tarelli R, Ferrari CC, Sarchi MI, Pitossi FJ. Fundación Instituto Leloir, FBMC-UBA, CONICET, Patricias Argentinas 435, (1405) Buenos Aires, Argentina. Parkinson's disease is a neurodegenerative disorder with uncertain aetiology and ill-defined pathophysiology. Activated microglial cells in the substantia nigra (SN) are found in all animal models of Parkinson's disease and patients with the illness. Microglia may, however, have detrimental and protective functions in this disease. In this study, we tested the hypothesis that a sub-toxic dose of an inflammogen (lipopolysaccharide) can shift microglia to a pro-inflammatory state and exacerbate disease progression in an animal model of Parkinson's disease. Central lipopolysaccharide injection in a degenerating SN exacerbated neurodegeneration, accelerated and increased motor signs and shifted microglial activation towards a pro-inflammatory phenotype with increased interleukin-1beta (IL-1beta) secretion. Glucocorticoid treatment and specific IL-1 inhibition reversed these effects. Importantly, chronic systemic expression of IL-1 also exacerbated neurodegeneration and microglial activation in the SN. In vitro, IL-1 directly exacerbated 6-OHDA-triggered dopaminergic toxicity. In vivo, we found that nitric oxide was a downstream molecule of IL-1 action and partially responsible for the exacerbation of neurodegeneration observed. Thus, IL-1 exerts its exacerbating effect on degenerating dopaminergic neurons by direct and indirect mechanisms. This work demonstrates an unequivocal association between IL-1 overproduction and increased disease progression, pointing to inflammation as a risk factor for Parkinson's disease and suggesting that inflammation should be efficiently handled in patients to slow disease progression. |
Rick
I was going to just hit the "thanks for this" button, but I just thought after all that effort to post you deserved a note of thanks. Of course I understood a beggers portion or it all, but shall re-read again. I think I need to go find the bottle of rum I hid somewhere after the last time I read research posted for our enlightenment. Can't we just eat a sound diet to get by? Apparently not.
Keep at er m'boy ...J |
dear rev...*smile
I have been dancing here for along time...
http://dl2.glitter-graphics.net/pub/...a3p74g0ror.gifhttp://dl6.glitter-graphics.net/pub/...iabt0kqd0n.gif LOL! |
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