[reverett123]

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]

[reverett123]

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]

[reverett123]

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]

[reverett123]

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.

[rosebud]

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

[lou_lou]

I have been dancing here for along time...




LOL!