I am considering adding stuff to my Brain Tonic to counter the toxic effects of DHMO.

It all depends on the response shown here to this urgent threat. More info below...

http://www.dhmo.org

http://www.dhmo.org/facts.html (GOOD threat presentation)

jackD

MS brains need lots of repair work because of the high rate of transected axons. (see below abstract)

jackD


N Engl J Med. 1998 Jan 29;338(5):278-85.

Axonal transection in the lesions of multiple sclerosis.

Trapp BD, Peterson J, Ransohoff RM, Rudick R, L.
SourceDepartment of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, OH 44195, USA.

Abstract
BACKGROUND: Multiple sclerosis is an inflammatory demyelinating disease of the central nervous system and is the most common cause of neurologic disability in young adults.

Despite antiinflammatory or immunosuppressive therapy, most patients have progressive neurologic deterioration that may reflect axonal loss.

We conducted pathological studies of brain tissues to define the changes in axons in patients with multiple sclerosis.

METHODS: Brain tissue was obtained at autopsy from 11 patients with multiple sclerosis and 4 subjects without brain disease. Fourteen active multiple-sclerosis lesions, 33 chronic active lesions, and samples of normal-appearing white matter were examined for demyelination, inflammation, and axonal pathologic changes by immunohistochemistry and confocal microscopy. Axonal transection, identified by the presence of terminal axonal ovoids, was detected in all 47 lesions and quantified in 18 lesions.

RESULTS: Transected axons were a consistent feature of the lesions of multiple sclerosis, and their frequency was related to the degree of inflammation within the lesion.

The number of transected axons per cubic millimeter of tissue averaged 11,236 in active lesions, 3138 at the hypocellular edges of chronic active lesions, 875 in the hypocellular centers of chronic active lesions, and less than 1 in normal-appearing white matter from the control brains.

CONCLUSIONS: Transected axons are common in the lesions of multiple sclerosis, and axonal transection may be the pathologic correlate of the irreversible neurologic impairment in this disease.

Comment in
N Engl J Med. 1998 Jan 29;338(5):323-5.
PMID: 9445407 [PubMed - indexed for MEDLINE]

Interesting stuff Jack.

From the second link in your original post:

“Although such clinical applications are a long way off, new understanding about how neurons survive and innervate their targets of communication is evolving at an ever-quickening pace.”

“There are numerous problems in using neurotrophic factors as therapeutics. Such a large quantity of neurons are responsive to them that systemic administration may well activate all kinds of axonal sprouts that are not desired. Perhaps high doses or chronic use could be mitogenic, increasing the risk of cancer. When neurotrophic factors have been administered experimentally to both animals and humans, some unexpected consequences have been observed including appetite suppression, weight loss, increased pain perception, and muscle aches.2 Thus, localized administration to the desired site of action, or site-selective actions of systemically administered neurotrophic factors, may be required if treatment is going to be safe.”

The concern that I have is based on the fact this line of research is in its infancy; and seems to be directed more toward manipulating a possible fault in the glutamate receptor in neuro-degenerative disease, and possibly finding a way to deliver NGF only to specific target areas.

Those approaches sound reasonable, as adding NGF indiscriminately could inhibit optosis of dysfunctional/diseased neurons, and actually cause them to grow. Aside from potentially allowing too much neuronal growth, that would have a devastating effect on those people who have undiagnosed brain cancers.

In addition, glutamate is necessary for normal function of the nervous system, because in addition to it acting as a principle neurotransmitter, it uses glutamate to produce Gaba. Glutamate is also used for function in other systems of the body. Inhibiting it may prove to be devastating.

Magnesium ions block glutamate receptors, so that may be a reason why so many MS patients find relief from symptoms by supplementing with magnesium and/or bathing in it (Epsom salts).

It seems like a safer bet for now may be to ensure that adequate levels of magnesium, (to possibly block some glutamate receptors), as well as Vitamin D3 (for production of NGF), are present, will provide the body with what it needs to help it maintain homeostasis naturally.

With love, Erika

Thank you Erika. A much nicer way of saying, what I was thinking.

It would be a great idea to just take a "MAGIC" Rx pill and lower our glutamate levels to save our axon/neurons. I do not think one exists.

There are numerous supplements that may do this job.

I have posted some of them and I will post more.

I would welcome any additional ones you folks can find.

jackD

Pflugers Arch. 2010 Jul;460(2):525-42. Epub 2010 Mar 14.

Glutamate receptors, neurotoxicity and neurodegeneration.

Lau A, Tymianski M.
SourceDivision of Applied and Interventional Research, Toronto Western Research Institute, 399 Bathurst Street, Toronto, ON, Canada, M5T 2S8.

Abstract
Glutamate excitotoxicity is a hypothesis that states excessive glutamate causes neuronal dysfunction and degeneration.

As glutamate is a major excitatory neurotransmitter in the central nervous system (CNS), the implications of glutamate excitotoxicity are many and far-reaching.

Acute CNS insults such as ischaemia and traumatic brain injury have traditionally been the focus of excitotoxicity research.

However, glutamate excitotoxicity has also been linked to chronic neurodegenerative disorders such as amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease and others.

Despite the continued research into the mechanisms of excitotoxicity, there are currently no pharmacological interventions capable of providing significant neuroprotection in the clinical setting of brain ischaemia or injury.

This review addresses the current state of excitotoxic research, focusing on the structure and physiology of glutamate receptors; molecular mechanisms underlying excitotoxic cell death pathways and their interactions with each other; the evidence for glutamate excitotoxicity in acute neurologic diseases; laboratory and clinical attempts at modulating excitotoxicity; and emerging targets for excitotoxicity research.

PMID: 20229265 [PubMed - indexed for MEDLINE]

This form of B-12 is very nuroprotective. methylcobalamin

I get mine 5 mg from www.lef.org and "eat them" all day long.

jackD

Eur J Pharmacol. 1993 Sep 7;241(1):1-6.

Protective effects of a vitamin B12 analog, methylcobalamin, against glutamate cytotoxicity in cultured cortical neurons.

Akaike A, Tamura Y, Sato Y, Yokota T.
SourceDepartment of Neuropharmacology, Faculty of Pharmacy and Pharmaceutical Sciences, ***uyama University, Japan.

Abstract
The effects of methylcobalamin, a vitamin B12 analog, on glutamate-induced neurotoxicity were examined using cultured rat cortical neurons. Cell viability was markedly reduced by a brief exposure to glutamate followed by incubation with glutamate-free medium for 1 h. Glutamate cytotoxicity was prevented when the cultures were maintained in methylcobalamin-containing medium.

Glutamate cytotoxicity was also prevented by chronic exposure to S-adenosylmethionine, which is formed in the metabolic pathway of methylcobalamin.

Chronic exposure to methylcobalamin and S-adenosylmethionine also inhibited the cytotoxicity induced by N-methyl-D-aspartate or sodium nitroprusside that releases nitric oxide. In cultures maintained in a standard medium, glutamate cytotoxicity was not affected by adding methylcobalamin to the glutamate-containing medium. In contrast, acute exposure to MK-801, a NMDA receptor antagonist, prevented glutamate cytotoxicity.

These results indicate that chronic exposure to methylcobalamin protects cortical neurons against NMDA receptor-mediated glutamate cytotoxicity.

PMID: 7901032 [PubMed - indexed for MEDLINE]

It appears that maintaining the PROPER levels of ZINC is also protective against glutamate neurotoxicity.


CAUTION!!! Too little ZINC is BAD and too much ZINC is VERY VERY BAD!!

jackD


Invest Ophthalmol Vis Sci. 1995 Sep;36(10):2048-53.

Protective action of zinc against glutamate neurotoxicity in cultured retinal neurons.

Kikuchi M, Kashii S, Honda Y, Ujihara H, Sasa M, Tamura Y, Akaike A.
SourceDepartment of Ophthalmology, Faculty of Medicine, Kyoto University, Japan.

Abstract
PURPOSE: To examine the effects of Zn2+ on glutamate-induced neurotoxicity in cultured retinal neurons.

METHODS: Primary cultures obtained from fetal rat retinas (16 to 19 days gestation) were used. The neurotoxic effects of excitatory amino acids were quantitatively assessed using the trypan blue exclusion method.

RESULTS: A brief exposure of retinal cultures to glutamate or N-methyl-D-aspartate (NMDA) induced delayed cell death. Zn2+ at concentrations of 3 to 30 microM ameliorated glutamate- and NMDA-induced neurotoxicity in a dose-dependent manner. By contrast, neurotoxicity induced by a 1-hour exposure to kainate was not affected by Zn2+.

CONCLUSIONS: These findings demonstrate that Zn2+ protects retinal neurons from NMDA receptor-mediated glutamate neurotoxicity.

PMID: 7657543 [PubMed - indexed for MEDLINE]

quercetin - neuroprotective role of quercetin

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

Brain Res. 2011 Apr 6;1383:289-99. Epub 2011 Jan 31.

The role of ASIC1a in neuroprotection elicited by quercetin in focal cerebral ischemia.

Pandey AK, Hazari PP, Patnaik R, Mishra AK.
SourceDivision of Cyclotron & Radiopharmaceutical Sciences, Institute of Nuclear Medicine and Allied Sciences, Brig SK Mazumdar Road, Delhi 110054, India.

Abstract
One of the major instigators to neuronal cell death and brain damage following cerebral ischemia is calcium dysregulation.

The intracellular calcium overload resulting from glutamate excitotoxicity is considered a major determinant for neuronal loss during cerebral ischemia. Moreover, ASIC1a activation due to acidosis also promotes intracellular calcium overload during ischemic insult.

Interestingly, ASIC1a was found to be inhibited by some flavonoids which carry an anti-inflammatory property particularly quercetin, which could be exploited in hypoxic conditions like cerebral ischemia.

This encourages us to investigate the neuroprotective effect of quercetin besides its possible downstream signaling mechanism in focal cerebral ischemia.

The treatment of quercetin 30min before ischemia and 4h after reperfusion shows significant protection from ischemic injury as noticed by reduction in cerebral infarct volume and neurobehavioral deficit. In addition to earlier calcium dependent rise in the levels of nitrite and MDA exhibited marked reduction (P<0.01) in their levels when given quercetin pretreatment in ischemic brain regions. The quercetin treatment also reduced the spectrin break down products (SBDP) caused by ischemic activation of calcium dependent protease calpain. In ex-vivo study, it was also observed that quercetin inhibited the acid mediated intracellular calcium levels in rat brain synaptoneurosomes.

These studies suggest the neuroprotective role of quercetin in focal cerebral ischemia by regulation of ASIC1a.Copyright © 2011 Elsevier B.V. All rights reserved.

PMID: 21281608 [PubMed - in process]

1: Biochem Pharmacol 2003 Mar 1;65(5):877-85

Flavonoids inhibit myelin phagocytosis by macrophages; a structure-activity relationship study.

Hendriks JJ, de Vries HE, van der Pol SM, van den Berg TK, van Tol EA, Dijkstra
CD.

Department of Molecular Cell Biology, VU Medical Centre, Van der Boechorststraat
7, 1081 BT, Amsterdam, The Netherlands.

Demyelination is a characteristic hallmark of the neuro-inflammatory disease multiple sclerosis. During demyelination, macrophages phagocytose myelin and secrete inflammatory mediators that worsen the disease.

Here, we investigated whether flavonoids, naturally occurring immunomodulating compounds, are able to influence myelin phagocytosis by macrophages in vitro.

The flavonoids luteolin, quercetin and fisetin most significantly decreased the amount of myelin phagocytosed by a macrophage cell line without affecting its viability. IC(50) values for these compounds ranged from 20 to 80 microM. The flavonoid structure appeared to be essential for observed effects as flavonoids containing hydroxyl groups at the B-3 and B-4 positions in combination with a C-2,3 double bond were most effective.The capacity of the various flavonoids to inhibit phagocytosis correlated well with their potency as antioxidant, which is in line with the requirement of reactive oxygen species for the phagocytosis of myelin by macrophages.

Our results implicate that flavonoids may be able to limit the demyelination process during multiple sclerosis.

PMID: 12628496 [PubMed - in process]

For the very interested reader here is the FULL TEXT>>> (THIS IS VERY GOOD STUFF FOR THE TRUELY PREVERTED)

TITLE: Flavonoids inhibit myelin phagocytosis by macrophages; a structure-activity relationship study.


http://home.ix.netcom.com/~jdalton/Flavonoids%20MS.pdf

jackD

Can't we just all eat right/healthy and get all the proper help our bodies
and brains need? I know, too simple and of course there are allergies
and diseases, that take away our ability to digest some of these good
foods.