Inflammation vs. neurodegeneration

If it's on your mind and it has to do with multiple sclerosis in any way, post it here.

Postby Lyon » Mon Jul 09, 2007 1:00 pm

Hi Harry,
Mindful that I'm treading in a thread belonging to the "other" guys, it doesn't help that none of the steroids or approved medications is anywhere near 100% effective at stopping myelin loss.

I'd quickly and willingly hop over to your side of the fence IF it was shown that any of the approved medications were effectively stopping myelin loss and yet disability progression continued.
Bob
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Postby HarryZ » Mon Jul 09, 2007 5:22 pm

Hi Bob,

Lyon wrote:Hi Harry,
Mindful that I'm treading in a thread belonging to the "other" guys, it doesn't help that none of the steroids or approved medications is anywhere near 100% effective at stopping myelin loss.

I'd quickly and willingly hop over to your side of the fence IF it was shown that any of the approved medications were effectively stopping myelin loss and yet disability progression continued.
Bob


As my wife's ex neuro told her a number of years ago...the MS community is quite disappointed that the CRAB drugs have not done what they expected they would do. The trial data from the companies lead the docs to believe that these drugs would be far more effective but we know that they weren't and still aren't.

Tysabri, according to Biogen, has better numbers but those stats came from mild MS patients and we don't know yet how effective this drug will be with more severe cases of the disease.

While associated with myelin loss, axonal damage seems to hold the answer to MS, whatever that may be. And watching axons deteriorate in the brain isn't exactly the easiest thing to study!!!

Harry
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Postby Lyon » Mon Jul 09, 2007 5:47 pm

HarryZ wrote: While associated with myelin loss, axonal damage seems to hold the answer to MS, whatever that may be. And watching axons deteriorate in the brain isn't exactly the easiest thing to study!!!
Hi Harry,
It might have been on this site where I recently read an article abstract which cautiously mentioned that axon loss might be the cause of MS disability.

Cripes! I don't know anything and I could have told them that one and they could have saved the time and effort on the study!
Bob
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Postby HarryZ » Mon Jul 09, 2007 7:50 pm

Hi Bob,

Cripes! I don't know anything and I could have told them that one and they could have saved the time and effort on the study!
Bob


It does seem perplexing sometimes, doesn't it but thinking something and medically proving it are two different commodities! That's why in the past I have challenged the auto-immune theory of MS because nobody has ever been able to prove it.

My wife Marg gets so frustrated when she hears about all the recent discoveries and ideas about MS. She says that's all very fine but it doesn't do one damn bit of good for me, does it? And you know....she's right!

Harry
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Postby robbie » Tue Jul 10, 2007 6:14 am

You have to believe, what ever the therapy and what ever that treatment is based on weather it be autoimmune or other , If you are involved with one of these drugs (lyon’s wife-tovaxin),(bromley-campath),(ancedote-antibiotics),(lyndacarol-insulin levels),(robbie-pot),(harrys wife-procarin),(muu-lamotrigine), what ever the drug what ever the reason for ms if you doing it you have to believe that you have made the right choise. We can argue about till were blue in the face but you have to defend your drug. I think what Harry’s wife said sums it all up for some of us anyway,
When someone has years of experience you tend to listen not only regarding ms but anything in life.

My wife Marg gets so frustrated when she hears about all the recent discoveries and ideas about MS. She says that's all very fine but it doesn't do one damn bit of good for me, does it? And you know....she's right!
Had ms for over 19 years now.
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Postby Lyon » Tue Jul 10, 2007 7:48 am

robbie wrote:When someone has years of experience you tend to listen not only regarding ms but anything in life.
Hi robbie,
Absolutely true.

Additionally, there is a world of difference in the needs of someone with more years experience and more disability than for someone with lesser disability who would be completely satisfied just (not that it's a minor achievement) to have disease progression stopped.

I don't believe it but a lot of researchers are of the opinion that SPMS might be a completely different "animal" than RRMS and for that reason alone people whose MS has progressed more have reason to feel that advances which benefit RRMS are not advances for them.

I have to admit that, at least in my case, what you've said is absolutely true. I'm so convinced about Tovaxin that it came to mind the other day that I've never even asked myself "what if Tovaxin doesn't work as well as I'm convinced it does/will?" and even then I didn't spend much time dwelling on it because I am and need to continue my conviction.

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Postby finn » Wed Jul 11, 2007 6:26 am

Wesley,
parts of your post went way over my head, so correct me if I have misunderstood it. I'd say instead of applying Matzinger's "danger model" you gave a possible explanation to an autoimmune reaction. If I got it right, there was no "danger" in your hypothesis, for some reason Alu sequenses just gave the immune system a reason to attack against own tissue. In any case, interesting post.

Sharon,
thanks for the andropause info. I'll need it soon :-)

Jack,
Trapp's study was important, but in it he studied only lesions. More recent studies have suggested that MS is a global disease of the CNS.

Bob,
Lyon wrote:I'd quickly and willingly hop over to your side of the fence IF it was shown that any of the approved medications were effectively stopping myelin loss and yet disability progression continued.
Maybe the day will come. Tysabri has already showed the poor correlation between inflammation, relapses and progression of disability. In the pivotal two year trial it could remove almost all inflammation seen as MRI-activity (92% less when compared to placebo), but there were still clinical relapses and a "risk" for disability.

robbie,
great post, thanks! You're right, everyone of us writing here seem to have an agenda. I personally have doubted the "inflammatory autoimmune disease" theory almost as long as I have had this disease. The idea of MS being a neurodegerative disease makes much more sense to me. It doesn't help me deal with my MS, though. The only relatively safe drug with neuroprotective potential I'd be interested to try (minocycline) is not available here in Finland.

Be well.

-finn
"The great tragedy of science - the slaying of a beautiful hypothesis by an ugly fact.” -Thomas Henry Huxley
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Postby Lyon » Wed Jul 11, 2007 7:42 am

finn wrote:Maybe the day will come. Tysabri has already showed the poor correlation between inflammation, relapses and progression of disability. In the pivotal two year trial it could remove almost all inflammation seen as MRI-activity (92% less when compared to placebo), but there were still clinical relapses and a "risk" for disability.
Hi finn,
Even though we all have our different viewpoints I think all of us equally will appreciate the day when some definite information appears...regardless of which way it goes.

I don't blame researchers for traditionally feeling that they need to draw conclusions from faulty and incomplete information. Otherwise we'd be asking them what they are doing with all those research dollars. On the other hand it seems that the biggest problem we face is that the world of MS is fraught with conclusions which have been drawn from faulty and incomplete information. Like you, maybe like most people, I have to wonder which, if any, commonly held assumptions about MS have any value at all. Which MS "truths" of today will remain "truths" in 5 or 10 years?

In reading that history of MS research the other day I was surprised and discouraged to read how long MS research has really been going on and how recently researchers have vacillated on information as seemingly simple as whether or not more women or men are affected with MS.

I guess my point is that in the world of MS, no "fact" is beyond reproach.

Bob
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Postby bromley » Wed Jul 11, 2007 1:20 pm

Finn,

I think this thread that you started has shown how complex and multi-faceted this disease is. The title of the thread is not quite right - neurodegeneration v inflammation. MS is a combination of neuro-degeneration and inflammation.

The chicken and egg issue (what comes first) is a really difficult one to pin down. Most cases of relapsing - remitting MS appear to have a high amount of inflammation at the start and more neuro-degeneration (and increasing disability) later in the disease course when there is less inflammation (and the disease is then classified as Secondary Progressive). Given this is the most common scenario, one can see why the researchers considered it to be a two-stage disease: an inflammatory disease followed by a neuro-degenerative disease.

When the disease is classified as Secondary Progressive, even the most powerful anti-inflammatories (such as Campath) cannot stop the neuro-degeneration (brain atrophy). So the researchers are testing the following theory: will the most powerful anti-inflammatories given early in the disease (RR course), prevent / radically slow down the neuro-degeneration that is seen later in the disease. Trials with drugs such as Campath and Mitoxantrone + copaxone should provide an answer, but it will be a number of years before we know.

A common view held by researchers is that the immune system attacks the myelin which surrounds the axons. The body tries to replace the myelin which supports the axons, but the repair eventually fails. This leads to axonal degeneration as the axon does not get the support it needs from the myelin and/or is exposed to the immune system attacks. However, I have seen a number of papers that suggest that it is the myelin making cells or the axons themselves (proteins on the axons) that may be the target of the immune attack. Why the immune system gets involved is still not known (although immune cells are in the CNS which shows that it is involved). It is still unclear what the immune system is seeking to do - and different parts of the immune system (T cells, B cells, T Reg cells) may be doing different things - attacking a virus, stimulating repair etc.

The two stage view of MS looks weak when PPMS is added to the picture. Here is a type of MS which appears to be about neuro-degeneration from the start. However, I have seen papers suggesting that there is lower grade inflammation and papers which state that even with PPMS there can be "attacks" during the disease course. Then there is Progressive Relapsing MS!

Some people experience much more benign MS where neuro-degeneration does not appear to be a major feature (at least for a very long time). This might suggest that MS is primarily an inflammatory disease which is followed (in some cases) by neuro-degeneration caused by the inflammation!

You are quite right to point out that the relationship between relapses and subsequent disease progression is not clear. But it is now recognised that for every clinical relapse, there are ten which the patient doesn't feel. This might suggest that there is alot of inflammation throughout the CNS doing damage and that the accumulation of this damage overburdens the system and the earlier damage leads to neuro-degeneration later on!

I am not trying to answer the what comes first - neurodegeneration or inflammation - question, but set out the complex cases that make this a difficult puzzle to crack.

Another complication to the picture is the age issue. On the whole, neuro-degenerative diseases (Parkinsons, dementias, ALS) come with older age. MS has been seen in very young children and strikes many around 30.

I hope that inflammation is the driver in most cases of MS as there are drugs which can pretty much address this (Campath, Mitoxantrone etc). I also hope that myelin or the myelin-making cells are the targets of the attack. Why? Because treatments to re-myelinate are in the pipeline (bone-marrow stem cells etc). If MS is, in fact, a neuro-degenerative disease (with inflammation as a response / side-show) then much of the research to date has been a waste of time. The researchers would need to find the reason for the neuro-degeneration and possible therapies. Some neuro-protective agents are being tested in trials - Lamotrigine and Cannaboids.

The next 12-18 months may well provide some answers. There should be more data on how well those treated with the powerful anti-inflammatories are doing (whether five or six years post treatment any patients have moved to the progressive stage i.e the anti-inflammatories had no effect on the neuro-degeneration). The Lamotrigine trial might report early findings i.e if the therapy slowed down brain atrophy. Perhaps most interesting is the Rituximab PPMS trial which is to report later this year or early next year. This should show whether depleting B cells has any effect on the progression of this form of the disease.

Sorry for the long post - I have no answers. But the more I think about it the more of a riddle MS becomes.

All the best

Ian
Last edited by bromley on Wed Jul 11, 2007 11:37 pm, edited 1 time in total.
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Postby Lyon » Wed Jul 11, 2007 1:30 pm

Good post Ian! You might just work your way back to hero status......providing those chocolates do eventually show up!
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Postby finn » Thu Jul 12, 2007 7:59 am

Ian,
I definitely agree with you on one thing, the pathology of MS is a combination of inflammation and neurodegeneration. We just seem to have complitely different opinions on the way those factors are connected.

Your neuro dr Giovannoni stated in a video presentation a couple of years ago that "inflammation defines the clinical course of MS". That's of course true. The more there is inflammation, the slower is the progression of permanent disability. To me it makes sense only if inflammation would be a reaction to neurodegeneration and its main task would be to protect nervous system and promote its repair. In that case reverseable demyelination caused by inflammation would be concidered only as "collateral damage".

Dr Giovannoni also stated that "RRMS and PPMS are the same disease". Animal studies have shown that when 15-30 % of axons are lost, first permanent clinical symptoms appear. It could mean that if MS starts as a slow neurodegenerative process, it could take years before it can be clinically diagnosed. And if inflammation would be a reaction to neurodegeneration, it could be involved in causing demyelination and complitely reverseable disability seen as relapses in RRMS (the recovery could be complete as long as the critical amount of axons is not destryed). In PPMS there would be no "protective" inflammatory phase, and thus it continues to progress after the diagnosis without remissions.

In my scenario treating inflammation with drugs would be ok as long as it doesn't have a negative effect on the neuroprotective properties of immune reaction in the long run. It could improve the quality of life by lessening the amount of relapses and allowing the CNS to remyelinate, but it couldn't stop the progression of neurodegeneration for good.

Be well.

-finn
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Postby bromley » Thu Jul 12, 2007 8:25 am

Finn,

I definitely agree with you on one thing, the pathology of MS is a combination of inflammation and neurodegeneration. We just seem to have complitely different opinions on the way those factors are connected.


We cannot have completely different opinions as I don't have an opinion. I hope that inflammation is the driving force that leads to neuro-degeneration, because there are drugs to address inflammation. If the experts cannot work out what comes first, then I cannot possibly have an opinion - what would I base it on?

You are of the opinion that MS is primarily a neuro-degenerative disease. I don't know if it is or is not. But this scenario means that there is no real hope for us, as we can do nothing about the neuro-degeneration. If this scenario is true, we are wasting our time injecting Rebif, Copaxone etc or getting on trials for therapies such as Tovaxin. This disease saps hope quickly, but I'd rather go out knowing I tried something (even if it made no difference) than do nothing.

Your opinion on MS being primarily a neuro-degenerative disease may be the right one, and may be proved so in the future. But I'm not interested in showing at the end of the day that my opinion (which I do not have on this issue) is right. My interest is in stopping relapses (my ones were very disabling) and getting as well as I can in the circumstances. My treatment choice is working well so far. You can only work with the tools we have at the moment and hope better ones are on their way. Unfortunately, opinions, even if they are proved right, do not get you better.

My other neuro Dr Coles thinks the following might be the way forward with MS treatments. He may be proved wrong, but it gives me hope.

Surely the future of multiple sclerosis treatment is the combination of:

1) a drug to stop all further immune attack (Campath-1H/mitoxantrone etc);

2) something to prevent axonal degeneration (perhaps lamotrigine); and

3) some manoeuvre to repair the damage already done (stem cells and the like)


Given that you have a strong view that MS is primarily a neuro-degenerative disease, what treatments options do you think offer hope? Do any of the treatments on trial (which Dignan has listed) offer any hope?

Ian
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Postby finn » Fri Jul 13, 2007 12:12 am

Ian,
for a man who has no opinion on this matter, you seem to have an awful lot to write about it ;-)

Well, you have already written almost the same post earlier in this thread. I answered you then that I understand and respect your point of view and decision to start taking Campath. Ì still do. I have also written that instead of "autoimmune" and "no autoimmune" camps people having opinion on this subject could be divided into "hope" and "scepticism" camps. I'm a natural born sceptic, but you obviously belong to the "hope" camp. That is why it might even be better for you to stop reading my posts. They probably won't give you hope or make you feel any better.

I started this thread because I think this is an extremely interesting topic. Even though I know it won't have a positive effect on my MS, I have enjoyed being involved in an intelligent debate over an extremely complicated issue. I like to read people sharing their opinions and showing with links and references what their thinking is based on. There is a huge amount of interesting information in this thread. Probably one day I'll sit back, have a glass of good wine, and read the whole thread through once more :-)

bromley wrote:Given that you have a strong view that MS is primarily a neuro-degenerative disease, what treatments options do you think offer hope? Do any of the treatments on trial (which Dignan has listed) offer any hope?

I'd say "hope" is a strong word to be used when we talk about a disease with unknown pathogenesis and treatments with more or less unspecific mode of action. Anyway, if we stick to drugs that have already reached phase III, I would probably put my money on MBP8298. It has worked quite well in SPMS and is now tested also in RRMS.

If I had the power, I would test the efficiency of minocycline in a large clinical trial against one of the ABCRs. I just read again the two year results of the Canadian minocycline trial and was still quite impressed. There were only ten people in the trial, but none of them had any MRI-activity nor relapses between months 6-24. It might not even matter if MS turns out to be an autoimmune or neurodegenerative disease, because minocycline seems to have both anti-inflammatory and neuroprotective properties ;-)

Be well.

-finn
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Postby jackD » Fri Jul 13, 2007 9:11 am

I believe in the BOTH theory.

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

Image

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Postby jackD » Fri Jul 13, 2007 9:36 am

I LOVE vinpocetine!!!

It make you smarter, stronger, harder, walk a lot better and piss like a "fire-hose" 8O .

jackD


VINPOCETINE HELPS MS PATIENTS

Exciting research with vinpocetine has been conducted on patients with multiple sclerosis. MS is a disease in which neural signals from the brain to the target muscle groups are obstructed because sclerotic plaques form in multiple locations along the nerve fibers and interrupt the signal transmission. As a result, the muscles weaken, and MS patients are often tired. In the later stages of the disease, they are often unable to walk, and they lose other motor skills as well.

MS patients treated with phosphodiesterase inhibitors, or PDEIs (see the sidebar for a description of phosphodiesterases and their inhibitors), exhibit a dramatic decrease in relapse rate.5 In a study published in the journal Multiple Sclerosis, 12 patients were treated with a cocktail of three different PDEIs, including 15 mg/day of vinpocetine, for an average of 499 days (1.4 years). The other two ingredients were the anti-Alzheimer's drug propentofylline and the antiasthma drug theophylline.

"Vinpocetine has the most clinical
promise for the management of
vascular insufficiencies
involving the brain."

Before the treatment, the patients averaged 3.1 relapses per year. During the treatment period, however, the incidence of relapses was much lower: only 0.92 per year. Seven of the 12 patients reported no relapses during the treatment period, three had a decreased incidence of relapses, and two had the same incidence as before. Since there were two other ingredients in the treatment formula, one can't say that vinpocetine alone was responsible for these results, but it likely played an important role in reducing the patients' relapse rates.


8O I hate to say this but Vinpocetine is a Potassium channel blocker.

That is what 4-AP does it should help MS folks walk better.

1: Neurosci Behav Physiol. 1998 Mar-Apr;28(2):116-20.Links
Nootropic agent vinpocetine blocks delayed rectified potassium currents more strongly than high-threshold calcium currents.Bukanova YuV , Solntseva EI.
Science Research Institute of the Brain, Russian Academy, Medical Sciences, Moscow.

A two-microelectrode potential clamping method was used on isolated common snail neurons to measure high-threshold Ca2+ and delayed rectified K+ currents. Addition of the nootropic agent vinpocetine (VPC) to the bathing solution rapidly and reversibly inhibited both types of current. The effects of VPC were dose-dependent and were independent of the test stimulus voltage. Maximum blockade of the Ca2+ current averaged 27% at a VPC concentration of 600 microM. Maximum blockade of the K+ current averaged 76% at a VPC concentration of 30 microM. It is concluded that K+ channels are more likely targets of VPC than Ca2+ channels.

PMID: 9604212 [PubMed - indexed for MEDLINE]

It also help with the MS urination problm.

1: World J Urol 2001 Nov;19(5):344-50

Phosphodiesterase 1 inhibition in the treatment of lower urinary tract
dysfunction: from bench to bedside.

Truss MC, Stief CG, Uckert S, Becker AJ, Wefer J, Schultheiss D, Jonas U.

Urologische Klinik, Medizinische Hochschule, Hannover, Germany.
truss.michael@mh-hannover.de

Anticholinergic drugs are currently the therapy of choice to treat urgency and
urge incontinence. However, muscarinergic receptor blockers with adequate
selectivity for detrusor smooth muscle are not available. Also, in contrast to
the normal detrusor, the unstable detrusor neurotransmission seems to be at
least partially regulated by non-cholinergic (NANC) pathways. These factors may
explain the common side effects and the limited clinical efficacy of these
compounds. Specific modulation of intracellular second messenger pathways offers
the possibility of organ selective manipulation of tissue function, specifically
contraction and relaxation of smooth musculature. Because of their central role
in the intracellular regulation of smooth muscle tone phosphodiesterases (PDEs)
are an attractive pharmacological targets. The PDE 5 specific inhibitor
sildenafil (Viagra) has revolutionized the treatment of patients with erectile
dysfunction. Numerous other PDE inhibitors are currently under investigation for
the treatment of various disorders. We investigated the role of PDEs in human
detrusor smooth muscle. Our data demonstrate the presence of five PDE isoenzymes
in human detrusor and suggest, for the first time, that the cAMP pathway and the
calcium/calmodulin-stimulated PDE (PDE 1) are of functional importance in the
intracellular regulation in this tissue in vitro. In addition. initial clinical
data with the PDE 1 inhibitor vinpocetine in patients not responding to standard
anticholinergic therapy indicate a possible role for vinpocetine in the
treatment of urgency, urge incontinence and, possibly, low compliance bladder
and interstitial cystitis. The results of a larger randomized, double-blind,
placebo-controlled, multicenter trial with vinpocetine show a tendency in favor
of vinpocetine over placebo; however, statistically significant results were
documented for one parameter only. This might be due to the rather low dosage
chosen and the small sample size. Further studies are necessary and currently
underway to delineate the optimal dosage, indications and patient population.
Modulation of intracellular key enzymes effecting second messenger metabolism,
i.e. isoenzyme-selective PDE inhibition is a novel approach which possibly
avoids the limitations of anticholinergic therapy in patients with lower urinary
tract dysfunction.

PMID: 11760783 [PubMed - in process]


Vinpocetine

Vinpocetine improves mental function through:
1. Improving the utilisation of glucose within the brain.
2. Improving the utilisation of oxygen within the brain.
3. Increasing circulation of blood to the brain.
4. Increasing production of ATP within the brain.
5. Increasing the turnover of the neurotransmitters norepinephrine and
serotonin
6. Slowing deposit of lipofuscin pigment between brain nerve cells.

Vinpocetine is derived from vincamine an extract obtained from the periwinkle
plant. Although they have many similar effect Vinpocetine appears to have more
benefits and fewer adverse effects than vincamine. Adverse effects are rare, but
include hypotension, dry mouth, weakness, and tachycardia

Clinical studies have shown that it has a powerful stimulating effect on memory.
Vinpocetine as been shown to improve brain metabolism in the following ways. It
increases blood flow to the brain, and the rate of ATP production within the
brain (hence increasing the amount of energy available to the brain from ATP
action). Additionally the velocity of glucose and oxygen turnover within the
brain is expanded. As a result of the overall increase in activity of brain cell
metabolism the brain is able to retain a greater quantity of information and to
process that information faster.

Vinpocetine appears to combine many of the benefits of several other cognitive
enhancers. Clinical studies have found that in general Vinpocetine is better
than vincamine and in general is at least as good as Hydergine, xanthinol
nicotinate, meclophenoxate, niacin, and cyclandelate

Medically Vinpocetine is used in the treatment of cerebral circulatory disorders
including memory problems, stroke, aphasia, apraxia and dizziness as well as
sensorineural impairment of hearing. Additionally Vinpocetine is used to treat a
number of ophthalmologic disorders, with some improvement of visual acuity in
70% of the subjects.

Vinpocetine is particularly notable for its effect on short-term memory. In one
double-blind crossover study normal healthy volunteers demonstrated an
extraordinary improvement in short-term memory an hour after taking 40-mg of
Vinpocetine. The subjects showing a doubling of processing speed when receiving
Vinpocetine as against a placebo (Z, Subhan, I, Hindmarch,
"Psychopharmacological Effects of Vinpocetine in Normal Healthy Volunteers",
European Journal of Clinical Pharmacology 1985, Volume 28).

Adverse effects are rare, but include hypotension, dry mouth, weakness, and
tachycardia. Vinpocetine has no drug interactions, no toxicity, and is generally
very safe.

Dosage: One or two 5 mg tablets per day

I take my Vinpocetine with my Idebenone.

jackD


1: Neuropharmacology 1989 Jun;28(6):569-73

Idebenone and vinpocetine augment long-term potentiation in hippocampal slices
in the guinea pig.

Ishihara K, Katsuki H, Sugimura M, Satoh M.

Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kyoto
University, Japan.

The effects of idebenone and vinpocetine which reportedly prevent impairment of
learning and memory were studied in vitro, on the long-term potentiation of the
population spike in the pyramidal layer of CA3 region of slices of hippocampus
in the guinea pig. Idebenone (10(-9) M-10(-6) M) or vinpocetine (10(-7) M-10(-6)
M) significantly augmented long-term potentiation in the mossy fibre-CA3
pyramidal cell system, without any significant changes in population spikes in
the absence of tetanic stimulation. These results suggest that both drugs have
direct actions on the hippocampal neurones to augment long-term potentiation at
fairly small concentrations. Further, when the two drugs were applied together,
the augmenting effects were additive.

PMID: 2569175 [PubMed - indexed for MEDLINE]
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