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Drugs that promote myelination

rhigm22 benztropine multiple sclerosis benzatropine white matter myelin

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#1 h2o

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Posted 29 January 2014 - 12:28 AM


I have found two drugs that may help grow/repair myelin which is of course important in learning and memory. I am more interested in benztropine since it is already available and tested on humans. So, does anyone have any experience with it? It is also available orally, IM, and IV. Would taking it orally even cross the blood barrier?

1) benztropine - anti-cholinergic agent already on the market to treat Parkinson's disease has been recently re-discovered to regrow myelin in damaged cells

The loss of myelin causes affected neurons to fail to transmit faithfully the messages that should be passing along them, leading to sensory, visual and movement problems and, in severe cases, paralysis.
But, there is evidence that, if the immune assault can be curtailed, a population of dormant brain stem cells, called oligodendrocyte precursors, can replace the lost myelin-making oligodendrocytes, leading to the re-insulation of the neurons denuded by the disease symptomatic improvement.
However, these cells appear to be too few in number to adequately replace those lost to the immune attacks, so recovery is incomplete at best.
Now, by screening over 100,000 different drugs, a team in California have uncovered one that strongly stimulates the production of new myelin-producing cells, known as oligodendrocytes, leading to the repair of MS brain lesions.

Ironically, the drug identified by Scripps Institute scientist Luke Lairson and his colleagues, is benztropine, which has been used for years to treat tremor in people with Parkinson's Disease. As such, it is already licensed for human use.

Benztropine works by blocking the action of a nerve signalling chemical called acetyl choline, which also keeps the oligodendrocyte precursors cells that make myelin in a quiescent state.

Interrupting this suppressive signal with benzotropine awakens the stem cells, triggering them to multiply and turn into new oligodendrocytes.
The team made the discovery by incubating the precursor cells with drug molecules in a culture dish before looking for markers of myelin production.
Promising leads were then tested further by growing precursors cells alongside cultured neurons and looking for evidence of successful myelination. When benztropine emerged as the most powerful candidate tested, the team then administered the agent to mice with the rodent equivalent of MS.
Treated animals showed dramatic improvements in their symptoms, and, under the microscope, significant re-myelination had taken place. In some further tests, the team also administered a low dose of immune-suppressing drugs; given alongside the benztropine, this regimen resulted in an even larger clinical benefit.
The researchers nonetheless urge caution. They point out in their paper in Nature, where the work is published, that, "benztropine has significant neurological and psychiatric side effects," emphasizing that further preclinical and clinical evaluation will be needed before the findings can be translated to the clinic.


http://www.thenakeds...s/news/1000341/


2) rHIgM22 - a new antibody currently in a phase 1 trial

If successful, a new remyelinating antibody called rHIgM22 may help reverse nerve damage caused by MS.

In a collaboration between the Mayo Clinic and Acorda Therapeutics, Inc., a “first-in-human” trial of the drug rHIgM22 to repair nerve damage caused by multiple sclerosis (MS) is currently recruiting volunteers.
Earlier animal studies of rHIgM22 showed improvements in motor activity, meaning a possible reversal of disability. If successful, this could be a groundbreaking achievement, particularly for those with progressive forms of MS, for which there are no treatments currently available.

There are currently ten disease modifying therapies (DMTs) available that have been approved by the U.S. Food and Drug Administration (FDA). Several more are poised to hit the market soon. While these drugs have become more effective at slowing disease progression and reducing the number of attacks a person with MS might have, none are able to repair or regrow myelin once damage has been done. But that could soon change.
Moses Rodriguez, M.D., a neurologist specializing in MS at the Mayo Clinic, and his team initially identified rHIgM22, recognizing its ability to protect and stimulate the cells that make myelin, called oligodendrocytes.

“This remyelinating antibody, if successful in clinical trials and approved, would be a novel approach to treating people with chronic neurologic deficits from multiple sclerosis or other similar conditions,” said Rodriguez in an interview with Business Wire. “We are excited that this Mayo discovery is now being evaluated in people with MS to determine its therapeutic potential.”



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#2 MrHappy

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Posted 29 January 2014 - 10:15 AM

I'd be mighty careful with benztropine or any other anti-cholinergics. In this forum, there are other / less risky options to increase myelination - if you are interested?

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#3 lourdaud

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Posted 29 January 2014 - 11:01 AM

Wouldn't anti-cholinergics be the last thing you'd want? I'm on bupropion and this thread made me a bit worried http://www.longecity...-demyelination/

#4 mait

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Posted 29 January 2014 - 01:56 PM

Pregnenolone and melatonin should aid in this respect

The taiep (tremor, ataxia, immobility, epilepsy, and paralysis) myelin mutant displays a number of locomotor deficits. Taiep rat gait is characterized by shorter stride and step lengths as well as by larger stride widths. Thirty-day-old taiep mutants were placed under a regimen of daily hormone injections for 60 days. Animals in Condition 1 received melatonin, those in Condition 2 received pregnenolone sulfate, and those in a third control condition received injections of saline. Following the injections, each taiep mutant's gait was analyzed. The animals that received melatonin and pregnenolone displayed significantly larger stride and step lengths than did the controls. In addition, the animals that received hormones displayed shorter stride widths than did the controls. These experimental effects are consistent with a normalization of gait. Possible cellular mechanisms of this behavioral effect are discussed.


From: http://www.tandfonli...97#.UukHrrTN3HQ

#5 Olorin

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Posted 29 January 2014 - 07:14 PM

I have Multiple Sclerosis, and in addition to some of the things mentioned earlier in the thread I use the following for remyelination:

Lithium: http://www.ncbi.nlm....pubmed/22355115
Lion's Mane: http://www.ncbi.nlm....pubmed/12675022
Aspirin: http://www.ncbi.nlm....pubmed/23653362

I also take "Myelin Basic Protein", which according to the company that sells it "may benefit brain and nerve function (myelination) by providing the basic building blocks needed to maintain and support healthy nerve cells". :)
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#6 Jochen

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Posted 30 January 2014 - 02:03 PM

I also take "Myelin Basic Protein", which according to the company that sells it "may benefit brain and nerve function (myelination) by providing the basic building blocks needed to maintain and support healthy nerve cells". :)


how has this MBP been working for you?

That looks quite interesting maybe even for in 'healthy' individuals as well.

Thanks in advance and good luck with your MS journey

#7 Olorin

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Posted 30 January 2014 - 03:30 PM

how has this MBP been working for you?

That looks quite interesting maybe even for in 'healthy' individuals as well.

Thanks in advance and good luck with your MS journey


My approach to handling my MS is far from scientific, in that I don't take the time to trial each substance separately but rather try "everything" at once, so I'm unable to say how well any specific product has worked.

Since I started my experimentation I've had no new lesions, and have never felt better, so something must be working. :)

#8 Jochen

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Posted 30 January 2014 - 03:57 PM

how has this MBP been working for you?

That looks quite interesting maybe even for in 'healthy' individuals as well.

Thanks in advance and good luck with your MS journey


My approach to handling my MS is far from scientific, in that I don't take the time to trial each substance separately but rather try "everything" at once, so I'm unable to say how well any specific product has worked.

Since I started my experimentation I've had no new lesions, and have never felt better, so something must be working. :)


glad to hear!

what MBP brand are you taking?

#9 Olorin

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Posted 30 January 2014 - 06:15 PM

what MBP brand are you taking?

Cardiovascular Research Ltd., Ecological Formulas, Sphingolin (http://www.iherb.com...-Capsules/23537)

#10 h2o

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Posted 01 February 2014 - 01:58 AM

Wouldn't anti-cholinergics be the last thing you'd want? I'm on bupropion and this thread made me a bit worried http://www.longecity...-demyelination/

I'd be mighty careful with benztropine or any other anti-cholinergics.


Benztropine isn't just any anti-cholinergic. Out of 100,000+ chemicals screened by researchers, benztropine was one of the few that offered promise in stimulating myelin growth.

Bupropion belongs to a different subclass of anti-cholinergics than Benztropine. Beztropine is anti-muscarinic while bupropion is anti-nicotinic. I tried bupropion in the past, and it really didn't do anything to help mood or cognition. It only had a stimulant effect for the first few days and then later I experienced this mildly strange sensation that didn't help at all.

If anyone is interested in the original research paper published in Nature, it is available here:

A regenerative approach to the treatment of multiple sclerosis

It appears that taking benztropine in oral form would cross the BBB:

" Among the most effective inducers of OPC differentiation was benztropine which we chose to investigate further because it is an orally available
approved drug that readily crosses the blood–brain barrier."

My understanding after reading that article is that the animals received therapeutic benefit after only 6 days.

There are risks and benefits to most pharmaceutics, and benztropine is approved for people 4 and older and pregnant women are told they can still take it with caution so it cannot be that bad. I can always taper off if the side effects are unbearable.

If anyone knows of a good source for 2mg benztropine tablets, please pm me.

Edited by h2o, 01 February 2014 - 02:00 AM.


#11 normalizing

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Posted 02 February 2014 - 02:12 AM

benztropine does look pretty interesting. i think most of you gus are too cautious about it without a good reason. i checked for any serious adverse reactions from regular use and i couldnt find problems. it has been approved and use for many years it seems. either way, you will need doctor to RX it h2o and that will be real difficult. how would you convience the doc to give it to you ? it kind of ruins it. and i believe its pricey too to take it long term anyway.

#12 h2o

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Posted 03 February 2014 - 03:18 PM

either way, you will need doctor to RX it h2o and that will be real difficult. how would you convience the doc to give it to you ? it kind of ruins it. and i believe its pricey too to take it long term anyway.


Benztropine is actually very reasonable pricewise. It has been around since the 1950s, making it widely available and affordable. I have seen it offered for about $50 or less for 60 2mg tablets. Anyone starting out would probably cut those 2mg tablets in halves or even fourths (daily dosage is 0.5 to 2mg) so that would cut costs even more.

But yeah, unless you have a diagnosis of Parkinson's getting a legit rx would be difficult. But as they say, if there's a will, there's a way. There are always loopholes.

#13 adamh

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Posted 04 February 2014 - 09:12 PM

There are internet pharmacies which will sell all sorts of things. I dont know of any off the top of my head that carry this, if its a very low volume product many places will not handle it. But if they do, it eliminates the need for an rx and all you have to worry about is customs grabbing it.

#14 h2o

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Posted 08 February 2014 - 02:53 PM

Thanks to cylack, another drug can be added to this list: clemastine. Clemastine is available OTC as an allergy drug so availability is not a problem. There is currently an active human trial going to investigate whether this drug will remyelinate axons in MS patients: http://clinicaltrial...ow/NCT02040298

More information can be found here: http://www.medpageto...ews_2014-02-06

Unlike the other drugs mentioned however, clemastine has no animal studies showing that it can promote myelination. It has only been shown in cultured cells in a petri dish to promote growth.

#15 formergenius

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Posted 08 February 2014 - 03:08 PM

IIRC, IGF-1 promotes myelination. See here.

#16 normalizing

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Posted 16 February 2014 - 08:54 PM

IGF-1 also promotes cancerogenesis
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#17 h2o

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Posted 27 March 2014 - 11:56 PM

Today is my 40th day on clemastine and I wanted to share my experiences. It was just a few months ago that the possible nootropic benefits of clemastine were published so relatively few people have tried it for this reason.

As you may know, clemastine is a generic OTC medication for allergies (e.g. sneezing and runny nose) so who would of thought that such a drug can potentially transform the brain at high doses!

Clemastine is currently being tested as a remyelinating agent for multiple sclerosis in clinical trials. The dosing in clinical trials is 4mg twice a day. After seeing what my reaction was for the first few days, I matched my dosing to those trials. Typical clemastine tablets (such as these) contain 1mg of active ingredient per one 1.34mg tablet. This means that to match the MS trial, you must take 8 of those small pills each day. I take 4mg of clemastine in the morning, and 4mg right before bed. On the label it says that you shouldn't take more than 2 pills every 24 hours but this indication of improving brain function is of course "experimental."

One of the major side effects of clemastine is drowsiness but paradoxically excitability may occur in some populations, especially children. Considering that I have pre-existing chronic fatigue (mental and physical), this side effect was worrying so I planned on remedying this effect with regular doses of modafinil. MS patients also have chronic fatigue so researchers are paying special attention to this symptom in the trials.

On the first day of clemastine, I did NOT experience drowsiness but instead the paradoxical excitability. I was more "wired" less "tired." Horary I thought. I should note that for the previous year I have been taking regular choline supplements. I found that I experienced benefits from choline alone, but for the clemastine trial I stopped those choline supplements cold turkey. I don't know if taking choline with an anti-cholinergic is a good idea. (Maybe someone here can chime in.)

The following days, the excitability calmed down. I didn't really experience the daytime drowsiness that I had strongly anticipated. During the first week, there were two times I felt the need to take a short nap but it was more like a "power nap" where I would lay down for 20 minutes and then I was good to go.

One thing that is noteworthy about my clemastine trial is that while I didn't feel drowsy during the day, I had a tendency to sleep 10 or more hours (more times than not). One Sunday I slept for 16 hours! When I wake up after those long sleeping durations, I feel thoroughly rested. I get the same type of well rested feeling that I got when I took melatonin. (I developed a quick tolerance to melatonin though, but clemastine's effects don't seem to go away with time for me). When I look back I think about all the time "wasted" sleeping when I could be productive. I2 hours is an awful lot of time to sleep, but then again the hope is that clemastine stimulates white matter formation, and it is during sleep that this process takes place. See Sleep 'boosts brain cell numbers'

I have found that clemastine is an effective anxiolytic. Additionally, I have noticed some positive subtle effects on cognition. The main reason I'm trying clemastine is to see whether it can help inattentive ADD (without hyperactivity). While ADHD (with hyperactivity) is mainly seen as a problem with inhibition, inattentive ADD is more of a true information processing with slow processing speed as one culprit. ADHD guru Dr. Barkley has compared the SCT type of attention problems as similar to those with white matter disease.

Research is coming out that while white matter dysfunction was been classically associated with neurological/autoimmune diseases, other conditions have also been implication. See White matter in learning, cognition and psychiatric disorders

Noninvasive brain imaging is revealing structural differences in appropriate white matter tracts in association with a wide range of neurological and psychiatric illnesses, including dyslexia, ADHD, depression, bipolar disorder, language disorders, stuttering, autism, obsessive-compulsive disorder, posttraumatic stress disorder, cognitive decline in aging, Alzheimer’s disease, Tourette’s disorder, schizophrenia and such idiosyncratic disorders as tone deafness and pathological lying.


White matter growth occurs naturally during learning new material and experiencing novel life events.

Learning complex skills, such as playing the piano, are accompanied by increased organization of white matter structure in appropriate brain tracts involved in musical performance [26]. Importantly, the level of white matter structure increased proportionately to the number of hours each subject had practiced the instrument, indicating white matter changes in acquiring the skill rather than performance being predetermined by a limitation on white matter development. Myelin plasticity might provide another cellular mechanism of learning complementing the well-studied mechanisms of synaptic plasticity.


For this reason, I picked up my dusty electric guitar that I don't play too often. One interesting thing is that I usually play the guitar sitting down because I don't lack the energy to stand for long periods, but between my second and third week I found myself standing up for long sessions and not thinking anything of it. It wasn't until later on did I realize that I didn't feel the urge to sit down after a few minutes. So yeah, cool observation but nothing too suggestive just yet of clemastine working the way I want it too.

Even if clemastine doesn't turn out to be the myelinating agent that everyone had hoped, at least it has a positive effect on sleep. (Usually I don't feel well rested after getting even 10 hours of sleep.) That in and of itself is beneficial in my opinion. I plan on continuing my clemastine trial for 90 days to see if I experience further benefits (but I may reduce the dose) and I think it is worth looking into as a nootropic.
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#18 normalizing

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Posted 29 March 2014 - 10:25 PM

its anticholinergic. i dont think thats a good idea to use it too long

#19 ChrisseyCoco

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Posted 07 May 2014 - 07:51 PM

I have tried Clemastine at 6mg once a day.  It has a feel good effect because it is an older antihistamine.  Since it only showed up in a High throughput screening,  I don't think that it is that effective in remyelination.  So I stopped taking it after 3 weeks because of stomach problems.

 

Since benztropine had more research done, I would also like to do a 3 week test of it but it seems impossible to get without a prescription.  So I tried to find a close cousin to this drug and found orphenadrine.  Orphenadrine is available OTC in Canada as an oral tablet 100mg.  I was able to order this.  Are there any opinions about orphenadrine?

 

I also am very interested in rHigM22 for remyelination but you need to get on a clinical trial to try that and they are only allowing patients who are already in their clinics. 

 

I have SPMS and I am new member.  So hello to everybody.



#20 normalizing

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Posted 07 May 2014 - 08:43 PM

^ how can you experiment with those anyway. how would you know if they are promoting myelination anyway since i suppose one way to find out is CT scans and such, also, you have to have some kind of a damage to be easily spotted...



#21 Luminosity

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Posted 08 May 2014 - 03:32 AM

It is important to ask if drugs are the best way to do this?  I would avoid things that demyelinize, such as artificial sweeteners, sodas, acidic food and drink, caffiene, for some, as well as wheat or glutinous grains, for some.  Food additives might do it for some people.  For a few people even turmeric, green tea, large doses of bromelain, or some other blood thinning or anti-oxidant supplements may attack their myelin.     


Edited by Luminosity, 08 May 2014 - 03:33 AM.


#22 swolo

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Posted 08 May 2014 - 05:20 AM

Would any of these affect myelination outside of the brain? I have nerve damage due to a cycling injury and am looking for anything that might help.



#23 Olorin

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Posted 08 May 2014 - 05:44 AM

It is important to ask if drugs are the best way to do this?  I would avoid things that demyelinize, such as artificial sweeteners, sodas, acidic food and drink, caffiene, for some, as well as wheat or glutinous grains, for some.  Food additives might do it for some people.  For a few people even turmeric, green tea, large doses of bromelain, or some other blood thinning or anti-oxidant supplements may attack their myelin.     

 

Turmeric/Curcumin, EGCG (Green tea) and even coffee do have medical research pointing in the direction of these being beneficial (in the right amounts) for Multiple Sclerosis - reducing demyelination, so this is interesting to me. Do you have any references I could take a look at where Turmeric, Green Tea or antioxidants has shown to contribute to demyelination? (I have Multiple Sclerosis, RRMS)



#24 normalizing

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Posted 08 May 2014 - 07:08 PM

^ he called them blood thinners. not sure i ever heard of them being blood thinners....



#25 Luminosity

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Posted 10 May 2014 - 01:06 AM

I'm not a he.  Yeah, they can thin blood.  Yes they can affect myelin outside the brain.  I said that those things can negatively effect myelin in some people.  My source is personal experience and also many people of this site have had adverse reactions to those things.   You can do a google search for those posts.  Not all the adverse reactions would be demyelinization specifically.  

 

People have different constitutions and different energy patterns, yin and yang and so forth.  That can cause some substances to go to certain parts of their bodies instead of where they want them to.  


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#26 Logic

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Posted 14 June 2016 - 01:23 PM

...The team, who published the study in Nature, wanted to find a drug that would encourage stem cells in the brain and spinal cord to become the type of cell that produces myelin, which are called oligodendrocytes. With more myelinating cells on board, the damage to nerve cells should slow down, and hopefully further damage will also be prevented. Ideally, the candidate drug would even start to reverse paralysis in multiple sclerosis sufferers.
The two drugs used in the trial were miconazole, which is found in over-the-counter antifungal treatments such as athlete’s foot, and clobetasol, which is used to treat skin conditions such as eczema...

http://drugplus.info...nerve-damage-2/


Edited by Logic, 14 June 2016 - 01:24 PM.


#27 gamesguru

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Posted 14 June 2016 - 07:01 PM

Polyphenols from green tea prevent antineuritogenic action of Nogo-A via 67-kDa laminin receptor and hydrogen peroxide.
Gundimeda U1, McNeill TH, Barseghian BA, Tzeng WS, Rayudu DV, Cadenas E, Gopalakrishna R. (2015)

Axonal regeneration after injury to the CNS is hampered by myelin-derived inhibitors, such as Nogo-A. Natural products, such as green tea, which are neuroprotective and safe for long-term therapy, would complement ongoing various pharmacological approaches. In this study, using nerve growth factor-differentiated neuronal-like Neuroscreen-1 cells, we show that extremely low concentrations of unfractionated green tea polyphenol mixture (GTPP) and its active ingredient, epigallocatechin-3-gallate (EGCG), prevent both the neurite outgrowth-inhibiting activity and growth cone-collapsing activity of Nogo-66 (C-terminal domain of Nogo-A). Furthermore, a synergistic interaction was observed among GTPP constituents. This preventive effect was dependent on 67-kDa laminin receptor (67LR) to which EGCG binds with high affinity. The antioxidants N-acetylcysteine and cell-permeable catalase abolished this preventive effect of GTPP and EGCG, suggesting the involvement of sublethal levels of H2 O2 in this process. Accordingly, exogenous sublethal concentrations of H2 O2 , added as a bolus dose (5 μM) or more effectively through a steady-state generation (1-2 μM), mimicked GTPP in counteracting the action of Nogo-66. Exogenous H2 O2 mediated this action by bypassing the requirement of 67LR. Taken together, these results show for the first time that GTPP and EGCG, acting through 67LR and elevating intracellular sublethal levels of H2 O2 , inhibit the antineuritogenic action of Nogo-A. Currently, several agents are being evaluated for overcoming axonal growth inhibitors to promote functional recovery after stroke and spinal cord injury. Epigallocatechin-3-gallate (EGCG), present in green tea polyphenol mixture (GTPP), prevents antineuritogenic activity of Nogo-A, a myelin-derived axonal growth inhibitor. The preventive action of EGCG involves the cell-surface-associated 67-kDa laminin receptor and H2 O2 . GTPP may complement ongoing efforts to treat neuronal injuries.

Flavonoids inhibit myelin phagocytosis by macrophages; a structure-activity relationship study.
Hendriks JJ1, de Vries HE, van der Pol SM, van den Berg TK, van Tol EA, Dijkstra CD. (2003)

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.

Promoting Myelination in an In Vitro Mouse Model of the Peripheral Nerve System: The Effect of Wine Ingredients
Mark Stettner,1,* Kathleen Wolffram,1 Anne K. Mausberg (2003)

Protective properties of moderate wine consumption against cancers, cardiovascular, metabolic and degenerative diseases have been reported in various clinical studies. Here, we analysed the effect of red wine (RW) and white wine (WW) on myelination using an in vitro embryonic co-culture mouse model. The total amount of myelin was found to be significantly increased after RW and WW treatment, while only RW significantly increased the number of internodes. Both types of wine increased rat Schwann cell- (rSC) expression of the NAD+-dependent deacetylase sirtuin-two-homolog 2 (Sirt2), a protein known to be involved in myelination.

Detailed chemical analysis of RW revealed a broad spectrum of anthocyanins, piceids, and phenolics, including resveratrol (RSV). In our assay system RSV in low concentrations induced myelination. Furthermore RSV raised intracellular glutathione concentrations in rSCs and in co-cultures and therefore augmented antioxidant capacity.

We conclude that wine promotes myelination in a rodent in vitro model by controlling intracellular metabolism and SC plasticity. During this process, RSV exhibits protective properties; however, the fostering effect on myelinaton during exposure to wine appears to be a complex interaction of various compounds.



#28 normalizing

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Posted 14 June 2016 - 08:25 PM

i know wine does this as it enhances mental clarity, concentration etc. but it seems to upregulate something because once you stop it, it all falls back down and its a difficult task to raise it again with anyhing ever, even with wine, tolerance occurs



#29 gamesguru

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Posted 14 June 2016 - 08:38 PM

how much do you have to drink? its my understanding the resveratrol content is actually laughable, and obviously after a point the drunkenness takes over. but I think this indicates more for extracts or supplements than wine drinking. i hear moderate alcohol consumption itself is good for the mind, so you could easily mistake that for the negligible polyphenol content

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#30 normalizing

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Posted 15 June 2016 - 02:29 AM

gamesguru, this is only a partial list https://en.wikipedia...s_found_in_wine there is so much stuff in wine, you will get dizzy trying to find all the information and comprehend it. its not just the resveratrol and definitely not the alcohol content as i have been trying many different types of alcoholic baverages, wine was the only one to not cause change in perception solely based on ethanol metabolism alone.







Also tagged with one or more of these keywords: rhigm22, benztropine, multiple sclerosis, benzatropine, white matter, myelin

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