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ALS / PLS and LDN

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> > >

> > Hi Mike, below is an out take on naloxone being used as a possible

> > treatment for brain diseases, ALS being one. I see the paper as an

> > independant report on how LDN could be real. Until there is

> clinical

> > data on how LDN effects people with a serious disease, we are doing

> > our own experiments. Hope Dr. Jill and Dr. Myra Gironi can

> > provide positve reports. The report below sort of confirms naloxone

> > (naltrexone) could help, at least in rats. My guess is that one

> should

> > be on LDN for about a year before you can get a sense if you're

> > holding your own (unless you're getting worse and then what do you

> > do?). Where did you get your LDN and how much were you taking? Did

> > your symptoms change after you stopped LDN?

> >

> >

> > OPIOIDS, BRAIN INFLAMMATION, AND...

> > REFERENCES

> >

> > Increasing evidence has suggested that inflammation in the brain is

> > closely associated with the pathogenesis of several degenerative

> > neurologic disorders, including Parkinson's disease, Alzheimer's

> > diseases, multiple sclerosis, amyotrophic lateral sclerosis, and

> AIDS

> > dementia. The hallmark of brain inflammation is the activation of

> > glial cells, especially that of microglia that produce a variety of

> > proinflammatory and neurotoxic factors, including cytokines, fatty

> > acid metabolites, free radicals—such as nitric oxide (NO) and

> > superoxide. Excessive production of NO, as a consequence of nitric

> > oxide synthase induction in activated glia, has been attributed to

> > participate in neurodegeneration. Using primary mixed neuron-glia

> > cultures and glia-enriched cultures prepared from embryonic rodent

> > brain tissues, we have systemically studied the relationship

> between

> > the production of NO and neurodegeneration in response to

> stimulation

> > by the inflammagen lipopolysaccharide. This review summarizes our

> > recent findings on the kinetics of NO generation, the relative

> > contribution of microglia and astrocytes to NO accumulation, the

> > relationship between NO production and neurodegeneration, and

> points

> > of intervention along the pathways associated with NO generation to

> > achieve neuroprotection. We also describe our results relating to

> the

> > effect of several opioid-related agents on microglial activation

> and

> > neuroprotection. Among these agents, the opioid receptor antagonist

> > naloxone, especially its non-opioid enantiomer (+)-naloxone,

> promises

> > to be of potential therapeutic value for the treatment of

> > inflammation-related diseases.

> > http://www.annalsnyas.org/cgi/content/full/962/1/318

>

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  • 2 weeks later...

Hi ,

I had gotten the LDN frpm Skip's and immediatly began taking 4.5,

then went down to 3.0 as I was getting very spastic (legs muscles

were very shaky) when arising from bed in the morning.

I got my LDN from Skip's again on 2/15/06 and spoke with Skip after

hearing what everyone here was recommending. He said that I was

taking to much to fast and didn't take it for long enough.

He said I should take 1.5 for 30 days, then 3.0 for 30, then 4.5.

That is what I am doing this time.

Thanks for the info on the brain inflamation.

Mike

> >

> Hi Mike, below is an out take on naloxone being used as a possible

> treatment for brain diseases, ALS being one. I see the paper as an

> independant report on how LDN could be real. Until there is

clinical

> data on how LDN effects people with a serious disease, we are doing

> our own experiments. Hope Dr. Jill and Dr. Myra Gironi can

> provide positve reports. The report below sort of confirms naloxone

> (naltrexone) could help, at least in rats. My guess is that one

should

> be on LDN for about a year before you can get a sense if you're

> holding your own (unless you're getting worse and then what do you

> do?). Where did you get your LDN and how much were you taking? Did

> your symptoms change after you stopped LDN?

>

>

> OPIOIDS, BRAIN INFLAMMATION, AND...

> REFERENCES

>

> Increasing evidence has suggested that inflammation in the brain is

> closely associated with the pathogenesis of several degenerative

> neurologic disorders, including Parkinson's disease, Alzheimer's

> diseases, multiple sclerosis, amyotrophic lateral sclerosis, and

AIDS

> dementia. The hallmark of brain inflammation is the activation of

> glial cells, especially that of microglia that produce a variety of

> proinflammatory and neurotoxic factors, including cytokines, fatty

> acid metabolites, free radicals—such as nitric oxide (NO) and

> superoxide. Excessive production of NO, as a consequence of nitric

> oxide synthase induction in activated glia, has been attributed to

> participate in neurodegeneration. Using primary mixed neuron-glia

> cultures and glia-enriched cultures prepared from embryonic rodent

> brain tissues, we have systemically studied the relationship

between

> the production of NO and neurodegeneration in response to

stimulation

> by the inflammagen lipopolysaccharide. This review summarizes our

> recent findings on the kinetics of NO generation, the relative

> contribution of microglia and astrocytes to NO accumulation, the

> relationship between NO production and neurodegeneration, and

points

> of intervention along the pathways associated with NO generation to

> achieve neuroprotection. We also describe our results relating to

the

> effect of several opioid-related agents on microglial activation

and

> neuroprotection. Among these agents, the opioid receptor antagonist

> naloxone, especially its non-opioid enantiomer (+)-naloxone,

promises

> to be of potential therapeutic value for the treatment of

> inflammation-related diseases.

> http://www.annalsnyas.org/cgi/content/full/962/1/318

>

> > I posted a last week in regards to PLS and LDN. There have been

no

> > responses. Does that mean nobody is familiar with PLS and LDN?

> >

> > PLS is in the same " family " as ALS, are there any persons who

have

> > used LDN who have ALS and have had any success?

> >

> > I had taken LDN for 1 1/2 months last year, but I had such a

worsening

> > of symptoms I stopped. I was afraid that if I kept taking LDN

things

> > would just continue to worsen, but I'd like to investigate it

more vs.

> > just giving up entirely.

> >

> > Thanks,

> >

> > Mike

> >

>

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Hi ,

I had gotten the LDN frpm Skip's and immediatly began taking 4.5,

then went down to 3.0 as I was getting very spastic (legs muscles

were very shaky) when arising from bed in the morning.

I got my LDN from Skip's again on 2/15/06 and spoke with Skip after

hearing what everyone here was recommending. He said that I was

taking to much to fast and didn't take it for long enough.

He said I should take 1.5 for 30 days, then 3.0 for 30, then 4.5.

That is what I am doing this time.

Thanks for the info on the brain inflamation.

Mike

> >

> Hi Mike, below is an out take on naloxone being used as a possible

> treatment for brain diseases, ALS being one. I see the paper as an

> independant report on how LDN could be real. Until there is

clinical

> data on how LDN effects people with a serious disease, we are doing

> our own experiments. Hope Dr. Jill and Dr. Myra Gironi can

> provide positve reports. The report below sort of confirms naloxone

> (naltrexone) could help, at least in rats. My guess is that one

should

> be on LDN for about a year before you can get a sense if you're

> holding your own (unless you're getting worse and then what do you

> do?). Where did you get your LDN and how much were you taking? Did

> your symptoms change after you stopped LDN?

>

>

> OPIOIDS, BRAIN INFLAMMATION, AND...

> REFERENCES

>

> Increasing evidence has suggested that inflammation in the brain is

> closely associated with the pathogenesis of several degenerative

> neurologic disorders, including Parkinson's disease, Alzheimer's

> diseases, multiple sclerosis, amyotrophic lateral sclerosis, and

AIDS

> dementia. The hallmark of brain inflammation is the activation of

> glial cells, especially that of microglia that produce a variety of

> proinflammatory and neurotoxic factors, including cytokines, fatty

> acid metabolites, free radicals—such as nitric oxide (NO) and

> superoxide. Excessive production of NO, as a consequence of nitric

> oxide synthase induction in activated glia, has been attributed to

> participate in neurodegeneration. Using primary mixed neuron-glia

> cultures and glia-enriched cultures prepared from embryonic rodent

> brain tissues, we have systemically studied the relationship

between

> the production of NO and neurodegeneration in response to

stimulation

> by the inflammagen lipopolysaccharide. This review summarizes our

> recent findings on the kinetics of NO generation, the relative

> contribution of microglia and astrocytes to NO accumulation, the

> relationship between NO production and neurodegeneration, and

points

> of intervention along the pathways associated with NO generation to

> achieve neuroprotection. We also describe our results relating to

the

> effect of several opioid-related agents on microglial activation

and

> neuroprotection. Among these agents, the opioid receptor antagonist

> naloxone, especially its non-opioid enantiomer (+)-naloxone,

promises

> to be of potential therapeutic value for the treatment of

> inflammation-related diseases.

> http://www.annalsnyas.org/cgi/content/full/962/1/318

>

> > I posted a last week in regards to PLS and LDN. There have been

no

> > responses. Does that mean nobody is familiar with PLS and LDN?

> >

> > PLS is in the same " family " as ALS, are there any persons who

have

> > used LDN who have ALS and have had any success?

> >

> > I had taken LDN for 1 1/2 months last year, but I had such a

worsening

> > of symptoms I stopped. I was afraid that if I kept taking LDN

things

> > would just continue to worsen, but I'd like to investigate it

more vs.

> > just giving up entirely.

> >

> > Thanks,

> >

> > Mike

> >

>

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