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Better myelination = faster nerve impulses

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#1 Mixter

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Posted 18 March 2009 - 02:23 PM


More Evidence That Intelligence Is Largely Inherited: Researchers Find That
Genes Determine Brain's Processing Speed

ScienceDaily (Mar. 18, 2009) — They say a picture tells a thousand stories,
but can it also tell how smart you are? Actually, say UCLA researchers, it

In a study published recently in the Journal of Neuroscience, UCLA neurology
professor Paul Thompson and colleagues used a new type of brain-imaging
scanner to show that intelligence is strongly influenced by the quality of
the brain's axons, or wiring that sends signals throughout the brain. The
faster the signaling, the faster the brain processes information. And since
the integrity of the brain's wiring is influenced by genes, the genes we
inherit play a far greater role in intelligence than was previously thought.

#2 Mixter

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Posted 18 March 2009 - 02:27 PM

So, what is the rate limiting step in myelinisation? The B12/folate dependent enzymes?

From http://www.lef.org/p...lerosis_02.htm:

Vitamin B12. Vitamin B12 plays a key role in the generation of myelin. Studies have shown that patients with MS often have abnormally low levels of vitamin B12 in their cerebrospinal fluid and/or blood serum (Reynolds EH 1992). In fact, clinical vitamin B12 deficiency and MS share remarkably similar characteristics, occasionally rendering correct diagnosis difficult (Miller A et al 2005). For more than three decades, many physicians have prescribed vitamin B12 injections for patients who have MS. Patients who have received vitamin B12 supplements have reportedly experienced consistent clinical improvements in their symptoms (Kidd PM 2001).

In the United Kingdom , researchers investigated the effects of 6 months of vitamin B12 injections (1 mg/week) on 138 patients with MS, in a double-blind, placebo-controlled, randomized study. Patients were assessed using a standardized evaluation of neurological disability. Although the treatment regimen also included the eventual addition of two other compounds, the researchers concluded that the conditions of patients with MS improved after starting vitamin B12 injections (Wade DT et al 2002).

They recommend up to 40mg B12 for Multiple Sclerosis treatment, but that would probably not benefit anyone with already healthy myelinisation?


Perhaps cAMP elevation may be a better target? Which could mean anything cAMP elevating like Forskolin, modified to pass the blood brain barrier, could be a potential myelination-enhancing nootropic.


Elevation of cAMP can overcome myelin inhibitors to encourage regeneration of the CNS. We show that a consequence of elevated cAMP is the synthesis of polyamines, resulting from an up-regulation of Arginase I, a key enzyme in their synthesis. Inhibiting polyamine synthesis blocks the cAMP effect on regeneration. Either over-expression of Arginase I or exogenous polyamines can overcome inhibition by MAG and by myelin in general. While MAG/myelin support the growth of young DRG neurons, they become inhibitory as DRGs mature. Endogenous Arginase I levels are high in young DRGs but drop spontaneously at an age that coincides with the switch from promotion to inhibition by MAG/myelin. Over-expressing Arginase I in maturing DRGs blocks that switch. Arginase I and polyamines are more specific targets than cAMP for intervention to encourage regeneration after CNS injury.

Edited by mixter, 18 March 2009 - 02:31 PM.

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#3 meursault

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Posted 18 March 2009 - 04:06 PM

Found this after a quick search...seems relevant, but I don't understand it much at all. Thought you might be interested anyway.
Constitutively Active Akt Induces Enhanced Myelination in the CNS

The serine/threonine kinase Akt regulates multiple cellular functions. The current studies identify a new role for Akt in CNS myelination. In earlier studies on cultured oligodendrocytes, we showed that neuregulin signals through phosphatidylinositol-3'-OH kinase and Akt to enhance survival of oligodendrocytes. However, when transgenic animals were generated that overexpressed constitutively active Akt in oligodendrocytes and their progenitor cells, no enhanced survival of oligodendrocytes or progenitors was found. No alteration in the proliferation or death of progenitors was noted. In contrast, the major impact of Akt overexpression in oligodendrocytes was enhanced myelination. Most interestingly, oligodendrocytes in these mice continued actively myelinating throughout life. Thus, expression of constitutively active Akt in oligodendrocytes and their progenitor cells generated no more oligodendrocytes, but dramatically more myelin. The increased myelination continued as these mice aged, resulting in enlarged optic nerves and white matter areas. In older animals with enlarged white matter areas, the density of oligodendrocytes was reduced, but because of the increased area, the total number of oligodendrocytes remained comparable with wild-type controls. Interestingly, in these animals, overexpression of Akt in Schwann cells did not impact myelination. Thus, in vivo, constitutively active Akt enhances CNS myelination but not PNS myelination and has no impact developmentally on oligodendrocyte number. Understanding the unique aspects of Akt signal transduction in oligodendrocytes that lead to myelination rather than uncontrolled proliferation of oligodendrocyte progenitor cells may have important implications for understanding remyelination in the adult nervous system.

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#4 Mixter

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Posted 29 March 2009 - 01:45 PM


B12 + Folate + Lecithin = key non-enzymatic things required for myelin synthesis,

BUT: Myelin Basic Protein is another rate-limitng factor (Ref: http://www3.intersci...97282/abstract)

Apparently, a synthesized fragment of MBP, Dirucotide may be able to emulate the essential functions of MBP. It is being used as treatment for MS. Together with the cofactors, this could be an interesting target for early therapy of other neurodegenerative diseases (myelin is always damaged first AFAIK) and as a nootropic.

Refs on Dirucotide:

1. Warren KG, Catz I, Ferenczi LZ, Krantz MJ. Intravenous synthetic peptide MBP8298 delayed disease progression in an HLA Class II-defined cohort of patients with progressive multiple sclerosis: results of a 24-month double-blind placebo-controlled clinical trial and 5 years of follow-up treatment. Eur J Neurol. 2006;13:887-95. PMID 16879301]
2. Holtbecker J. Detektion von bovinem Nervengewebe als spezifiziertes Risikomaterial in Fleischerzeugnissen durch Etablierung eines speziesspezifischen ELISA für die Routinediagnostik unter Verwendung des Myelin Basic Protein. Inaug Diss. 2004. LMU München: Tierärztliche Fakultät

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