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Microgial activation, Antibiotics, ALS, etc....

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Are there certain antibiotics that have been found to be more

effective than others in shutting down microglial activation? I

understand these are the immune cells in the brain, which produce

free radicals and cytokines when activated. When this activation

inappropiately continues for long periods (as can happen after

vaccination, apparently), you get chronic illness.

I've read that Garth Nicholson has had success with this kind of

treatment in people with Gulf War Syndrome. Do you know of a good

forum where his work is discussed?

When you all talk about antibiotics, are you generally thinking of

the anti-inflammatory and immune-modulating effects of them in

addition to their bug-killing capabilities? (I'm trying to catch up

here...)

The info and link below from Mycoplasm Registry group mentions this

in terms of ALS and Minocycline.

MycoplasmaRegistry/message/145

2: Neurobiol Dis 2002 Aug;10(3):268-78

Minocycline slows disease progression in a mouse model of amyotrophic

lateral sclerosis.

Kriz J, Nguyen MD, n JP.

Centre for Research in Neurosciences, McGill University, Research

Institute of the McGill University Health Centre, Montreal, Quebec,

H3G

1A4, Canada.

There is currently no effective pharmacological treatment for

amyotrophic

lateral sclerosis (ALS). Because recent evidence suggests that

secondary

inflammation and caspase activation may contribute to

neurodegeneration

in ALS, we tested the effects of minocycline, a second-generation

tetracycline with anti-inflammatory properties, in mice expressing a

mutant superoxide dismutase (SOD1(G37R)) linked to human ALS.

Administration of minocycline into the diet, beginning at late

presymptomatic stage (7 or 9 months of age), delayed the onset of

motor

neuron degeneration, muscle strength decline, and it increased the

longevity of SOD1(G37R) mice by approximately 5 weeks for

approximately

70% of tested mice. Moreover, less activation of microglia was

detected

at early symptomatic stage (46 weeks) and at the end stage of disease

in

the spinal cord of SOD1(G37R) mice treated with minocycline. These

results indicate that minocycline, which is clinically well tolerated,

may represent a novel and effective drug for treatment of ALS. PMID:

12270689 [PubMed - indexed for MEDLINE]

---------------------------------------------------

3: Neuroreport 2002 Jun 12;13(8):1067-70

Minocycline delays disease onset and mortality in a transgenic model

of

ALS.

Van Den Bosch L, Tilkin P, Lemmens G, Robberecht W.

Laboratory for Neurobiology, Campus Gasthuisberg, Herestraat 49, B-

3000

Leuven, Belgium.

Microglial activation is thought to contribute to the progression of

selective motor neuron death during amyotrophic lateral sclerosis

(ALS).

As minocycline has been shown to inhibit microglial activation, the

therapeutic efficacy of this tetracycline derivative in the G93A mice

model for familial ALS was tested. This drug with proven safety

delayed

disease onset and dose-dependently extended the survival of the G93A

mice. At 120 days of age, minocycline protected mice from loss of

motor

neurons and from vacuolization. These results demonstrate that

interference with immuno-inflammatory responses has a beneficial

effect

in the ALS mice model, suggesting this to be a potential new strategy

to

treat ALS. PMID: 12060810 [PubMed - indexed for MEDLINE]

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