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Old 06-24-2008, 05:38 PM #1
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Default NGF - Calcium - The Degenerative Stage of MS

Numerous neurotrophic growth factors help determine which neurons develop in the immature brain and which are retained in the adult brain.

Neurotrophic factors can also induce neurons to sprout axons capable of growing into new locations and forming new synaptic connections, a process that continues in the mature brain.

NGF (Nerve Growth Factor) is one essential neurotrophic growth factor. The below links describe how calcium is used in this process and how Glutamate toxicity kills neurons using Calcium in the Second stage of MS.


http://www.psychiatrist.com/pcc/brainstorm/br5904.htm (main article)

http://www.psychiatrist.com/pcc/brainstorm/br5906.htm (therapeutic potential)

http://www.psychiatrist.com/pcc/brainstorm/br5806.htm (Glutamate assassin/excitotoxic neuron murder)

The Second Stage of MS is "The Degenerative Stage" in which "excess Glutamate" runs wild on a killing spree. First phase, of course, is the "Inflammatory Stage" of MS.

http://home.ix.netcom.com/~jdalton/ms-two-stages.pdf

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Last edited by jackD; 06-24-2008 at 07:20 PM.
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Old 06-24-2008, 07:10 PM #2
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Quote:
Originally Posted by jackD View Post
Numerous neurotrophic growth factors help determine which neurons develop in the immature brain and which are retained in the adult brain.

Neurotrophic factors can also induce neurons to sprout axons capable of growing into new locations and forming new synaptic connections, a process that continues in the mature brain.

NGF (Nerve Growth Facto)r is one essential neurotrophic growth factor. The below links describe how calcium is used in this process and how Glutamate toxicity kills neurons using Calcium in the Second stage of MS.


http://www.psychiatrist.com/pcc/brainstorm/br5904.htm (main article)

http://www.psychiatrist.com/pcc/brainstorm/br5906.htm (therapeutic potential)

http://www.psychiatrist.com/pcc/brainstorm/br5806.htm (Glutamate assassin/excitotoxic neuron murder)

The Second Stage of MS is "The Degererative Stage" in which "excess Glutamate" runs wild on a killing spree. First phase, of course, is the "Inflammatory Stage" of MS.

http://home.ix.netcom.com/~jdalton/ms-two-stages.pdf

jackD

Thanks, Jack for all your good information on the subject.
__________________
Diagnosed Probable MS 9/21/07
.

Started Copaxone 10/16/07


3-6-9 the goose drank wine the monkey chewed tobacoo on the street car line the line broke the monkey got choked and they all went to heaven in a little row boat...
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Old 06-24-2008, 08:21 PM #3
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Hi jackD! You are making want to go to the library and get a biochem book!! I am sure I got rid of my college book when it was 25 years old.

I am concerned that NGF also influences the activity of B and T cells. I would have to understand how a little better.

I did find vitamin D3 at BJs Wholesale Club in 1000 IU capsules. I understand why we may need more.

I very much liked your last link because it had the best graphic explaining the nerve issues with the chemicals and how Copaxone works in certain situations.If anyone has a little knowledge about biochem you really should take a peek.

I don't know how you are finding this material, in its complete form, but I am glad you are sharing it. Its not easy to find more than just an abstract.

I know that our dendrites can grow and elongate,

http://www-als.lbl.gov/als/science/s...9receptor.html

and that is why my neuro told me about Wii actually helping to grow these for folks who can't get enough activity outside of the home.

So to keep this back to Vitamin D, it supports the NGF, if I am interpretting this properly.
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Old 06-24-2008, 08:31 PM #4
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Originally Posted by starfish View Post
Hi jackD! You are making want to go to the library and get a biochem book!! I am sure I got rid of my college book when it was 25 years old.

I am concerned that NGF also influences the activity of B and T cells. I would have to understand how a little better.

I did find vitamin D3 at BJs Wholesale Club in 1000 IU capsules. I understand why we may need more.

I very much liked your last link because it had the best graphic explaining the nerve issues with the chemicals and how Copaxone works in certain situations.If anyone has a little knowledge about biochem you really should take a peek.

I don't know how you are finding this material, in its complete form, but I am glad you are sharing it. Its not easy to find more than just an abstract.

I know that our dendrites can grow and elongate,

http://www-als.lbl.gov/als/science/s...9receptor.html

and that is why my neuro told me about Wii actually helping to grow these for folks who can't get enough activity outside of the home.

So to keep this back to Vitamin D, it supports the NGF, if I am interpretting this properly.
THANKS!!

You are right about the Vit D and NGF connection.

That techie site...

http://www.copewithcytokines.de/cope.cgi?key=NGF

says that ...
Quote:
Serum, phorbol 12-myristate 13-acetate (see also: Phorbol esters), and vitamin D3 are potent inducers of NGF synthesis. Glucocorticoids inhibit the synthesis of NGF.
.

That comment about Glucocorticoids (STEROIDS) blocking NGF production is a real bummer.

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Old 06-24-2008, 08:54 PM #5
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Default idebenone - NGF

I also take some IDEBENONE to get some extra NGF production in my brain. It is a bit expensive and you need to take 2 caps daily.

jackD

p.s. It a modified form of CQ-10 and is somewhat difficult to find in stores. I hear the rats love the stuff. I can now make it thru the water maze in a flash.

Quote:
1: Naunyn Schmiedebergs Arch Pharmacol. 1994 Apr;349(4):401-7.

Oral administration of idebenone induces nerve growth factor in the brain and improves learning and memory in basal forebrain-lesioned rats.

Nitta A, Murakami Y, Furukawa Y, Kawatsura W, Hayashi K, Yamada K, Hasegawa T, Nabeshima T.

Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University School of Medicine, Japan.

Nerve growth factor plays an important role in the survival and maintenance of cholinergic neurons in the central neuronal system. In senile dementia of the Alzheimer type, learning and memory are impaired by the loss of neurons in the magnocellular cholinergic neuronal system.

It is therefore, of interest to investigate the role of nerve growth factor in this degenerative disorder.

Since nerve growth factor does not cross the blood-brain barrier and is easily metabolized by peptidases when administered peripherally, it can be used for medical treatment only when directly injected into the brain.

We demonstrate here that the oral administration of idebenone, a potent in vitro nerve growth factors synthesis stimulator, induced an increase in nerve growth factor protein and mRNA, and in choline acetyltransferase activity, in basal forebrain lesioned rats, but not in intact rats.

Idebenone also ameliorated the behavioral deficits in habituation, water maze, and passive avoidance tasks in these animals.

These results suggest that idebenone stimulated nerve growth factor synthesis in vivo and ameliorates the behavioral deficits which were accompanied with the recovery of the reduced choline acetyltransferase activity in the basal forebrain-lesioned rats.

PMID: 8058112 [PubMed - indexed for MEDLINE]
Quote:
1: Zh Nevrol Psikhiatr Im S S Korsakova. 2008;108(4):27-32.Links
[Noben (idebenone) in the treatment of dementia and memory impairment without dementia][Article in Russian]


[No authors listed]
Noben (idebenone) was administered in dosage 120 mg during 6 months to 35 patients, aged from 60 to 86 years, with dementia, Alzheimer's type and mixed type, and with memory disturbances which did not reach the level of dementia. The assessment of patient's state before and after treatment was based on the results of somatic, neurological and psychiatric examination as well as neuropsychological testing and using of psychometrical and other scales. The significant improvement on the MMSE scale was found in patients with mild and moderate dementia.

The improvement of daily activity was observed in 27% of patients. The neuropsychological study revealed the improvement of short-term and delayed memory and attention, speech functions, the performance on kinesthetic, spatial and dynamic praxis tests, visual-spatial gnosis, reasoning and writing.

The positive therapeutic effect assessed by the CGI scale was observed in 37% of patients, the stable state--in 48%.

PMID: 18454094 [PubMed - in process]

Last edited by jackD; 06-25-2008 at 10:56 AM.
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Old 06-25-2008, 10:53 AM #6
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Default Other reason for taking Vit (K1 & K2) combo

Not a bad side effect for something that stops/removes excess calcium deposits from Vit D/calcium supplementing.

jackD


Quote:
1: J Neurosci. 2003 Jul 2;23(13):5816-26.

Novel role of vitamin k in preventing oxidative injury to developing oligodendrocytes and neurons.

Li J, Lin JC, Wang H, Peterson JW, Furie BC, Furie B, Booth SL, Volpe JJ, Rosenberg PA.
Department of Neurology, Division of Neuroscience, Children's Hospital, Boston, MA 02115, USA.

Oxidative stress is believed to be the cause of cell death in multiple disorders of the brain, including perinatal hypoxia/ischemia.

Glutamate, cystine deprivation, homocysteic acid, and the glutathione synthesis inhibitor buthionine sulfoximine all cause oxidative injury to immature neurons and oligodendrocytes by depleting intracellular glutathione.

Although vitamin K is not a classical antioxidant, we report here the novel finding that vitamin K1 and K2 (menaquinone-4) potently inhibit glutathione depletion-mediated oxidative cell death in primary cultures of oligodendrocyte precursors and immature fetal cortical neurons with EC50 values of 30 nm and 2 nm, respectively. The mechanism by which vitamin K blocks oxidative injury is independent of its only known biological function as a cofactor for gamma-glutamylcarboxylase, an enzyme responsible for posttranslational modification of specific proteins. Neither oligodendrocytes nor neurons possess significant vitamin K-dependent carboxylase or epoxidase activity. Furthermore, the vitamin K antagonists warfarin and dicoumarol and the direct carboxylase inhibitor 2-chloro-vitamin K1 have no effect on the protective function of vitamin K against oxidative injury.

Vitamin K does not prevent the depletion of intracellular glutathione caused by cystine deprivation but completely blocks free radical accumulation and cell death.

The protective and potent efficacy of this naturally occurring vitamin, with no established clinical side effects, suggests a potential therapeutic application in preventing oxidative damage to undifferentiated oligodendrocytes in perinatal hypoxic/ischemic brain injury.

PMID: 12843286 [PubMed - indexed for MEDLINE
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Old 06-25-2008, 01:59 PM #7
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Default NGF & Vit K1 K2 & neurons

Interesting to see how NGF and the Vit Ks work together to protect and enhance neuron outgrowth.

jackD


Quote:
Neurosci Lett. 2002 Apr 19;323(1):9-12.

Novel effect of vitamin K(1) (phylloquinone) and vitamin K(2) (menaquinone) on promoting nerve growth factor-mediated neurite outgrowth from PC12D cells.

Tsang CK, Kamei Y.
Marine and Highland Bioscience Center, Saga University, 152-1 Shonan-cho, Karatsu, 847-0021, Saga, Japan.


The nerve growth factor (NGF)-potentiating effect of K vitamins on PC12D cells was investigated.

Treatment of PC12D cells with vitamin K(1) or K(2) in the presence of NGF significantly enhanced the proportion of neurite-bearing cells and acetylcholinesterase activity compared with NGF treatment alone.

The K vitamins-enhanced neurite outgrowth on PC12D cells was completely blocked by a protein kinase A (PKA) inhibitor or mitogen-activated protein kinase (MAPK) kinase inhibitor PD98059, whereas a protein kinase C inhibitor chelerythrine chloride did not significantly inhibit the enhancing effect of the K vitamins.

These results suggest that the K vitamins enhance neurite outgrowth via the activation of PKA and MAPK-mediated signaling pathways in PC12D cells.

PMID: 11911978 [PubMed - indexed for MEDLINE]
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