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Best Supplements to Stimulate Neurotrophic Factors

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#61 nidhogg

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Posted 10 December 2011 - 10:53 AM

As far as selegiline and and nerve growth factor goes, i wouldnt bet any money on it.


We investigated the effects of selegiline and desmethylselegiline on synthesis of neurotrophic factors in cultured mouse astrocytes. Treatment with 2 mM selegiline for 24 h increased the contents of NGF, BDNF, and GDNF in the culture medium 26-, 1.7-, and 4.2-fold over the control, respectively. With this drug the maximum relative mRNA levels of NGF, BDNF, and GDNF were 6.2-fold at 2 h, 3.4-fold at 6 h, and 2.7-fold at 2 h, respectively. Selegiline at 0.2 mM completely inhibited the MAO activity, but had no effect on the content of neurotrophic factors, suggesting that stimulation of neurotrophic factors by selegiline is independent of MAO-B inhibition. Desmethylselegiline at 1.68 mM for 24 h elevated the NGF, BDNF, and GDNF contents 4.1-, 1.7-, and 2.4-fold over the control, respectively; and the relative transcript levels of NGF, BDNF, and GDNF reached 2.6-fold at 2 h, 1.7-fold at 6 h, and 1.8-fold at 2 h, respectively. These findings suggest that selegiline and desmethylselegiline may protect neurons by up-regulating endogenous NGF, BDNF, and GDNF synthesis.

http://www.ncbi.nlm.nih.gov/pubmed/11162424

With the doses people on these boards are taking i doubt even MAO is completely inhibited, and then 10x times that dose for NGF benefits.

Selegiline molar mass is 187.
2mM = 374mg/L, split in 12 for faster rat metabolic rate = 31mg/L, then taking bioavailability and human blood volume into consideration we can approximate 150mg/day to reap NGF benefits and 15mg/day to completely inhibit MAO

#62 computeTHIS

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Posted 10 December 2011 - 04:53 PM

[quote name='nito' timestamp='1323501668' post='490407']
[quote name='computeTHIS' timestamp='1323498036' post='490401']
[quote name='nito' timestamp='1323491906' post='490398']
[quote name='computeTHIS' timestamp='1323485229' post='490389']
[quote name='nito' timestamp='1322758216' post='488793']
Which method would stimulate NGF the fastest? Exercise, lions mane, ppq, or idebebone? Any takers?
[/quote]
I haven't tried Lion's Mane but I would suspect it's the most potent one of them all. Its cost is the reason I haven't given it a try, but I intend to try growing it sometime.

PQQ and Idebenone are both good, the effects are most noticeable on Idebenone before tolerance builds up. I'm not sure it's actually "tolerance" but rather its mental effects seem to follow a hyperbolic curve with neural growth/stimulation, at least that's my experience with it.
[/quote]

U reckon lions mane is quickest? i thought it took 6 months to feel NGF on lions mane. My guess was exercise. But if it's lions mane then i'm happily going to buy the liquid one.
[/quote]
Well, what you "feel" and what is actually a result from NGF may be two different things. Cognitive benefit from Idebenone happened in the same day for me, but I wouldn't attribute it to the action of NGF, rather, the associated stimulation from Idebenone's action on the mitochondria.

From my readings on it, Lion's Mane would appear to be the most potent one of them all, whether or not you feel it immediately. If you want something with immediate results, Idebenone will do it, and its benefits didn't subside after ceasing supplementation. It caused lasting cognitive improvements from only 4 days of use.

However, I've heard that some of the published work on Lion's Mane has represented a conflict of interest - where the author(s) stood to benefit from Lion's Mane sales. I also question the quality of available supplements, since the studies often involve more concentrated dosages and storage/preparation conditions could also affect potency - this is why I'm more interested in growing my own (it's also said to be easy to grow, with "plugs" of it sold online).
[/quote]

I've never given lions mane a propper long trial. I only gave it a month, but ill give liquid lions mane a go, pricey but worth a shot. Idebonone looks interesting. Is it smartpowders stuff you got?
[/quote]

Primaforce, 180mg. Can't remember which store, whichever one was cheapest off of Google shopping or something.

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#63 nidhogg

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Posted 11 December 2011 - 10:32 AM

The same study that links deprenyl to BDNF also states that they did not see any significant change in MAO inhibiting doses, but that BDNF release was induced by a dose 10x of complete MAO inhibition.

I.e. forget deprenyl unless you want to cross MAO-A inhibition aswell and start chewing on 100mg? ED
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#64 computeTHIS

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Posted 11 December 2011 - 11:46 AM

The same study that links deprenyl to BDNF also states that they did not see any significant change in MAO inhibiting doses, but that BDNF release was induced by a dose 10x of complete MAO inhibition.

I.e. forget deprenyl unless you want to cross MAO-A inhibition aswell and start chewing on 100mg? ED

Good point. Another study seems to suggest that the metabolite, L-methamphetamine, can actually inhibit cells from getting NGF (http://www.ncbi.nlm....pubmed/14732458).

Another study seems to show that Rasagiline tends to increase GDNF activity, whereas Selegiline increases BDNF activity (http://www.ncbi.nlm....pubmed/19673610).

Well, there's got to be a reason that Rasagiline is prescribed over Selegiline for PD, right? I look forward to Rasagiline going generic this February. From what I gather, people usually prefer Selegiline over Rasagiline, which I suspect has something to do with Selegiline's active metabolites.
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#65 nidhogg

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Posted 11 December 2011 - 12:49 PM

The same study that links deprenyl to BDNF also states that they did not see any significant change in MAO inhibiting doses, but that BDNF release was induced by a dose 10x of complete MAO inhibition.

I.e. forget deprenyl unless you want to cross MAO-A inhibition aswell and start chewing on 100mg? ED

Good point. Another study seems to suggest that the metabolite, L-methamphetamine, can actually inhibit cells from getting NGF (http://www.ncbi.nlm....pubmed/14732458).

Another study seems to show that Rasagiline tends to increase GDNF activity, whereas Selegiline increases BDNF activity (http://www.ncbi.nlm....pubmed/19673610).

Well, there's got to be a reason that Rasagiline is prescribed over Selegiline for PD, right? I look forward to Rasagiline going generic this February. From what I gather, people usually prefer Selegiline over Rasagiline, which I suspect has something to do with Selegiline's active metabolites.



Funny, you dont hear much about rasagiline. From the looks of it i find it superior over selegiline for cognitive purposes. But then again i prefer GDNF over BDNF

I assume its not available to the public due to the patent which may also contribute to its lack of popularity

#66 devinthayer

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Posted 12 December 2011 - 05:29 PM

The same study that links deprenyl to BDNF also states that they did not see any significant change in MAO inhibiting doses, but that BDNF release was induced by a dose 10x of complete MAO inhibition.

I.e. forget deprenyl unless you want to cross MAO-A inhibition aswell and start chewing on 100mg? ED

Good point. Another study seems to suggest that the metabolite, L-methamphetamine, can actually inhibit cells from getting NGF (http://www.ncbi.nlm....pubmed/14732458).

Another study seems to show that Rasagiline tends to increase GDNF activity, whereas Selegiline increases BDNF activity (http://www.ncbi.nlm....pubmed/19673610).

Well, there's got to be a reason that Rasagiline is prescribed over Selegiline for PD, right? I look forward to Rasagiline going generic this February. From what I gather, people usually prefer Selegiline over Rasagiline, which I suspect has something to do with Selegiline's active metabolites.



Funny, you dont hear much about rasagiline. From the looks of it i find it superior over selegiline for cognitive purposes. But then again i prefer GDNF over BDNF

I assume its not available to the public due to the patent which may also contribute to its lack of popularity


"PC12 is a cell line derived from a pheochromocytoma of the rat adrenal medulla. PC12 cells stop dividing and terminally differentiate when treated with nerve growth factor. This makes PC12 cells useful as a model system for neuronal differentiation." - Wikipedia

"Cultured PC-12 cells in absence of serum and nerve growth factor (NGF) die by an apoptotic process."

"However, while aminoindan (1 microM), the major metabolite of rasagiline does not interfere with the neuroprotective activities of rasagiline or selegiline in PC-12 cells deprived of serum and NGF, the major metabolite of selegiline, L-methamphetamine (1 microM), inhibits them."

L-methamphetamine inhibits the neuroprotective effects of rasagiline and selegiline in certain cases where NGF is deprived and typically required for survival. It does not block NGF... rather, it blocks the neuroprotection of Rasagiline and Selegiline. This is also not good, but there is a clear difference.

#67 devinthayer

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Posted 12 December 2011 - 06:48 PM

The same study that links deprenyl to BDNF also states that they did not see any significant change in MAO inhibiting doses, but that BDNF release was induced by a dose 10x of complete MAO inhibition.

I.e. forget deprenyl unless you want to cross MAO-A inhibition aswell and start chewing on 100mg? ED


Here is the study abstract:

Selegiline and desmethylselegiline stimulate NGF, BDNF, and GDNF synthesis in cultured mouse astrocytes.
We investigated the effects of selegiline and desmethylselegiline on synthesis of neurotrophic factors in cultured mouse astrocytes. Treatment with 2 mM selegiline for 24 h increased the contents of NGF, BDNF, and GDNF in the culture medium 26-, 1.7-, and 4.2-fold over the control, respectively. With this drug the maximum relative mRNA levels of NGF, BDNF, and GDNF were 6.2-fold at 2 h, 3.4-fold at 6 h, and 2.7-fold at 2 h, respectively. Selegiline at 0.2 mM completely inhibited the MAO activity, but had no effect on the content of neurotrophic factors, suggesting that stimulation of neurotrophic factors by selegiline is independent of MAO-B inhibition. Desmethylselegiline at 1.68 mM for 24 h elevated the NGF, BDNF, and GDNF contents 4.1-, 1.7-, and 2.4-fold over the control, respectively; and the relative transcript levels of NGF, BDNF, and GDNF reached 2.6-fold at 2 h, 1.7-fold at 6 h, and 1.8-fold at 2 h, respectively. These findings suggest that selegiline and desmethylselegiline may protect neurons by up-regulating endogenous NGF, BDNF, and GDNF synthesis.


For a 5mg dose, this is achievable, but not in a constant 24hrs. See ENSAM charts on study of bioavailability and why the invention of the Selegiline patch was made: http://selegiline.co...iline-EMSAM.pdf Page 4 for the graphs. It's much higher than 1.68nM of desmethylselegiline or 2nM of Selegiline.

Still, Rasagiline is better overall it may seem in terms of neuroprotection.

Edited by devinthayer, 12 December 2011 - 06:55 PM.


#68 nidhogg

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Posted 12 December 2011 - 07:33 PM

Not gonna bother reading that huge PDF file, but out of curiousity how do you figure that 2 millimolar equals 5mg?

Treatment with 2 mM selegiline for 24 h increased the contents of NGF, BDNF, and GDNF in the culture medium 26-, 1.7-, and 4.2-fold over the control, respectively. With this drug the maximum relative mRNA levels of NGF, BDNF, and GDNF were 6.2-fold at 2 h, 3.4-fold at 6 h, and 2.7-fold at 2 h, respectively. Selegiline at 0.2 mM completely inhibited the MAO activity, but had no effect on the content of neurotrophic factors, suggesting that stimulation of neurotrophic factors by selegiline is independent of MAO-B inhibition.


Disregarding any chemical knowledge, if 0.2 nM completely inhibited MAO and 5mg deprenyl ED doesnt even tap into the MAO A threshold, how exactly would one reap any of the effects?

Molar mass of selegiline is 187g. 2mM would equal 374mg/dm3 or litre.

Edited by nidhogg, 12 December 2011 - 07:35 PM.

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#69 devinthayer

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Posted 12 December 2011 - 09:15 PM

Not gonna bother reading that huge PDF file, but out of curiousity how do you figure that 2 millimolar equals 5mg?

Treatment with 2 mM selegiline for 24 h increased the contents of NGF, BDNF, and GDNF in the culture medium 26-, 1.7-, and 4.2-fold over the control, respectively. With this drug the maximum relative mRNA levels of NGF, BDNF, and GDNF were 6.2-fold at 2 h, 3.4-fold at 6 h, and 2.7-fold at 2 h, respectively. Selegiline at 0.2 mM completely inhibited the MAO activity, but had no effect on the content of neurotrophic factors, suggesting that stimulation of neurotrophic factors by selegiline is independent of MAO-B inhibition.


Disregarding any chemical knowledge, if 0.2 nM completely inhibited MAO and 5mg deprenyl ED doesnt even tap into the MAO A threshold, how exactly would one reap any of the effects?

Molar mass of selegiline is 187g. 2mM would equal 374mg/dm3 or litre.


Ah.... simple mistake. I've never seen mM in a study of significance. I read it quick and automatically assumed it was nanoMole, not milliMole. I had to double check that one. That's frickin' bogus. I can't believe they would even conclude that "selegiline and desmethylselegiline may protect neurons by up-regulating endogenous NGF, BDNF, and GDNF synthesis," without stating in some form the vast difference in plasma levels of Selegiline from normal use is a million times less than the concentrations they use in the study.

Desmethylselegiline Average Plasma Concentration for 10mg Oral:
67.7[ng-hr/mL]*10^(-9)[g/ng]*1000[mL/L]/187[g/mol] = 362nM-hr

Hey anyone have 2 grams of selegiline lying around?

Jk, jk...

Edited by devinthayer, 12 December 2011 - 10:13 PM.


#70 nidhogg

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Posted 12 December 2011 - 10:11 PM

Not to mention that the study was conducted on cultured mouse astrocytes. The test subjects would probably die in vivo from that dosage.

Not sure if its been mentioned before but heres something interesting:
http://en.wikipedia....wiki/Ladostigil

It acts as a reversible acetylcholinesterase and butyrylcholinesterase inhibitor, and an irreversible monoamine oxidase B inhibitor
In addition to its neuroprotective properties, ladostigil enhances the expression of neurotrophic factors like GDNF and BDNF, and may be capable of reversing some of the damage seen in neurodegenerative diseases via the induction of neurogenesis

Study

#71 computeTHIS

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Posted 13 December 2011 - 04:38 AM

Not to mention that the study was conducted on cultured mouse astrocytes. The test subjects would probably die in vivo from that dosage.

Not sure if its been mentioned before but heres something interesting:
http://en.wikipedia....wiki/Ladostigil

It acts as a reversible acetylcholinesterase and butyrylcholinesterase inhibitor, and an irreversible monoamine oxidase B inhibitor
In addition to its neuroprotective properties, ladostigil enhances the expression of neurotrophic factors like GDNF and BDNF, and may be capable of reversing some of the damage seen in neurodegenerative diseases via the induction of neurogenesis

Study

Yes, if I recall correctly, it's in stage III trials for Alzheimer's patients - still quite a ways from being generic, and hasn't even been considered yet for any other condition (that I know of). I feel as though Ladostigil represents some kind of great artistry in designer-pharmacology, and it's a bit sad that no company in the US has produced anything quite like it.

Edited by computeTHIS, 13 December 2011 - 04:39 AM.


#72 nidhogg

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Posted 13 December 2011 - 10:26 AM

Not to mention that the study was conducted on cultured mouse astrocytes. The test subjects would probably die in vivo from that dosage.

Not sure if its been mentioned before but heres something interesting:
http://en.wikipedia....wiki/Ladostigil

It acts as a reversible acetylcholinesterase and butyrylcholinesterase inhibitor, and an irreversible monoamine oxidase B inhibitor
In addition to its neuroprotective properties, ladostigil enhances the expression of neurotrophic factors like GDNF and BDNF, and may be capable of reversing some of the damage seen in neurodegenerative diseases via the induction of neurogenesis

Study

Yes, if I recall correctly, it's in stage III trials for Alzheimer's patients - still quite a ways from being generic, and hasn't even been considered yet for any other condition (that I know of). I feel as though Ladostigil represents some kind of great artistry in designer-pharmacology, and it's a bit sad that no company in the US has produced anything quite like it.



True, but on the other hand it doesnt have to be generic for people to get their hands on it, assuming demand is high enough. I know plenty of research chemicals far more complicated than a modified indane ring "leak" to the market before even hitting stage 3 trial.
A custom synthesis quote shouldnt cost much in this case.

Guess the question is whether or not someone with money really wants to experiment with experimental enzyme inhibitors.

#73 health_nutty

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Posted 16 December 2011 - 05:41 AM

Bump the best topic... ever.

#74 computeTHIS

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Posted 16 December 2011 - 05:54 AM

Not to mention that the study was conducted on cultured mouse astrocytes. The test subjects would probably die in vivo from that dosage.

Not sure if its been mentioned before but heres something interesting:
http://en.wikipedia....wiki/Ladostigil

It acts as a reversible acetylcholinesterase and butyrylcholinesterase inhibitor, and an irreversible monoamine oxidase B inhibitor
In addition to its neuroprotective properties, ladostigil enhances the expression of neurotrophic factors like GDNF and BDNF, and may be capable of reversing some of the damage seen in neurodegenerative diseases via the induction of neurogenesis

Study

Yes, if I recall correctly, it's in stage III trials for Alzheimer's patients - still quite a ways from being generic, and hasn't even been considered yet for any other condition (that I know of). I feel as though Ladostigil represents some kind of great artistry in designer-pharmacology, and it's a bit sad that no company in the US has produced anything quite like it.



True, but on the other hand it doesnt have to be generic for people to get their hands on it, assuming demand is high enough. I know plenty of research chemicals far more complicated than a modified indane ring "leak" to the market before even hitting stage 3 trial.
A custom synthesis quote shouldnt cost much in this case.

Guess the question is whether or not someone with money really wants to experiment with experimental enzyme inhibitors.


In a thread titled, "Ladostigil", some of us decided we were interesting in obtaining some. Quotes were never obtained though, China was likely the cheapest provider (not to mention the one with most chemical suppliers). Quotes usually don't cost anything, but you have to be representing your own company. Despite concerns over their quality, I'm fairly willing to rely on their purity reports. By all means though, if you obtain some quotes I'm sure you'll find some of us willing to go in on it.
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#75 gamesguru

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Posted 22 December 2011 - 03:23 AM

Ladostigil needs to be researched more.

Induction of neurotrophic factors GDNF and BDNF associated with the mechanism of neurorescue action of rasagiline and ladostigil: new insights and implications for therapy.
Weinreb O, Amit T, Bar-Am O, Youdim MB.
Source
Department of Pharmacology, Rappaport Family Research Institute, Technion-Faculty of Medicine, P.O. Box 9697, 31096 Haifa, Israel.
Abstract
Parkinson's disease (PD) and Alzheimer's disease (AD) are the most common neurodegenerative disorders, although there is no drug or therapeutic treatment to demonstrate disease-modifying effects. Previous work has proposed that neurodegeneration is linked to a lack of trophic support in those neurons and brain areas associated with PD and AD. Indeed, previous studies have found that neurotrophic factors (NTFs) support neuronal survival in various cellular and animal models of PD and AD. Thus, attention has begun to turn to the possibility of NTF neuroprotective-neurorescue therapies for these diseases, indicating that NTFs may be of significant clinical importance as exogenously supplied or endogenously induced elements that obliterate neuronal deficits and degeneration. We have recently reported that the anti-PD drug rasagiline, the anti-AD drug ladostigil, and their propargyl moiety, propargylamine, enhanced the expression levels of brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor, endogenous NTFs associated with activation of phosphatidylinositol 3-kinase, protein kinase, and mitogen-activated protein kinase cell signaling/survival pathways. These studies indicate that the induction of NTFs by rasagiline and ladostigil might suppress apoptosis and induce neurorescue in neurodegenerative disorders and may support the drugs' possible disease-modifying mechanism of action.

→ source (external link)

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#76 health_nutty

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Posted 04 January 2012 - 10:53 PM

So now that we have discussed every substance, lets take the discussion to the next level?

1) Which substances have the best research behind them?
2) Which have the best value?
3) What is a sample regimine to stimulate nootropic factors(basic, intermediate, advanced)?

#77 nito

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Posted 08 January 2012 - 03:53 AM

So now that we have discussed every substance, lets take the discussion to the next level?

1) Which substances have the best research behind them?
2) Which have the best value?
3) What is a sample regimine to stimulate nootropic factors(basic, intermediate, advanced)?


good questions. Hopefully someone knowledgeable like chrono will give it an attempt.

#78 Austin Diablo

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Posted 08 January 2012 - 04:48 AM

I would add Cannabis to that list.


lol, i have never seen a very clever pothead


Joe Rogan is fairly clever (and funny) and he's a pothead...But he also endorses nootropics and takes a product he plugs on his podcasts regularly (along with the Fleshlight, which, btw, ROCKS lol!). I have heard and read that cannabis does actually target and kill brain cancer/tumors. So it can have some positive effects medicinally.
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#79 computeTHIS

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Posted 08 January 2012 - 07:14 AM

So now that we have discussed every substance, lets take the discussion to the next level?

1) Which substances have the best research behind them?
2) Which have the best value?
3) What is a sample regimine to stimulate nootropic factors(basic, intermediate, advanced)?


good questions. Hopefully someone knowledgeable like chrono will give it an attempt.

I think more research is needed before addressing these questions. I've seen no research (thus far) which quantifies the neurotrophic benefit of these substances in order to make comparisons.

These neurotrophic factors often seem to be tacked on in order to market supplements. In other words, "Daily value not yet established" and I doubt they want this kind of research to come to light, or else some manufacturers will be seeing serious losses.

#80 nito

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Posted 08 January 2012 - 09:33 AM

So now that we have discussed every substance, lets take the discussion to the next level?

1) Which substances have the best research behind them?
2) Which have the best value?
3) What is a sample regimine to stimulate nootropic factors(basic, intermediate, advanced)?


good questions. Hopefully someone knowledgeable like chrono will give it an attempt.

I think more research is needed before addressing these questions. I've seen no research (thus far) which quantifies the neurotrophic benefit of these substances in order to make comparisons.

These neurotrophic factors often seem to be tacked on in order to market supplements. In other words, "Daily value not yet established" and I doubt they want this kind of research to come to light, or else some manufacturers will be seeing serious losses.


i just started taking fungi perfect lions mane liquid. I then read some post about lions mane and cancer n it freaked me out lol. Have you taken the the fungi perfect liquid?

#81 Michael Campbell

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Posted 08 January 2012 - 04:19 PM

I would add Cannabis to that list.


lol, i have never seen a very clever pothead


Joe Rogan is fairly clever (and funny) and he's a pothead...But he also endorses nootropics and takes a product he plugs on his podcasts regularly (along with the Fleshlight, which, btw, ROCKS lol!). I have heard and read that cannabis does actually target and kill brain cancer/tumors. So it can have some positive effects medicinally.


He's also a moon landing denier, which puts him squarely in the "crackpot" category for me.

#82 computeTHIS

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Posted 09 January 2012 - 01:38 AM

i just started taking fungi perfect lions mane liquid. I then read some post about lions mane and cancer n it freaked me out lol. Have you taken the the fungi perfect liquid?

No, I haven't. What's the cancer report you found? I'm still waiting for the opportunity to grow my own Lion's Mane, rather than paying the ridiculous online prices for it.

#83 nito

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Posted 09 January 2012 - 07:05 PM

i just started taking fungi perfect lions mane liquid. I then read some post about lions mane and cancer n it freaked me out lol. Have you taken the the fungi perfect liquid?

No, I haven't. What's the cancer report you found? I'm still waiting for the opportunity to grow my own Lion's Mane, rather than paying the ridiculous online prices for it.


Chrono talks about it on this page http://www.longecity...f/page__st__240

#84 nito

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Posted 11 January 2012 - 05:20 AM

I sip on the fungi perfect like it was vodka. Im getting quite far down da bottle lol. Burns ur throat when u swallow it though.
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#85 LeonardElijah

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Posted 15 January 2012 - 07:01 PM

Great thread, THANKS! I really needed some sort of overview of growth factors.

I take a lot of this list already. I've been waiting like no other to get my hands on Magnesium-l-threonate. It's next on my list. Please keep the first post updated. I will check back.

#86 hippocampus

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Posted 20 February 2012 - 09:51 PM

Interesting reading:
http://blogs.scienti...ssant-response/

It says that higher BDNF levels predict better response to antidepressants. :)
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#87 gamesguru

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Posted 27 February 2012 - 05:39 PM

Some other potential neurotrophin-stimulators:

' class='bbc_url' title='External link' rel='nofollow external'>http://www.ncbi.nlm.nih.gov/pubmed/21145362']Oroxylin A increases BDNF production by activation of MAPK-CREB pathway in rat primary cortical neuronal culture.
Jeon SJ, Rhee SY, Seo JE, Bak HR, Lee SH, Ryu JH, Cheong JH, Shin CY, Kim GH, Lee YS, Ko KH.
Source
Department of Pharmacology, College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, San 56-1, Shillim-Dong, Kwanak-Gu, Seoul 151-742, Republic of Korea.
Abstract
Oroxylin A (5,7-dihydroxy-6-methoxyfavone) is a flavonoid compound originated from the root of Scutellaria baicalensis Georgi. Our previous reports suggested that oroxylin A improves memory function in rat, at least in part, by its antagonistic effects on GABA(A) receptor. In addition, oroxylin A protects neurons from ischemic damage by mechanisms currently not clear. In this study we determined whether oroxylin A modulates the level of brain derived neurotrophic factor (BDNF) in primary rat cortical neuronal culture, which is well known for its role on neuronal survival, neurogenesis, differentiation of neurons and synapses and learning and memory. Treatment of oroxylin A for 3-48h increased BDNF expression which was analyzed by ELISA assay and Western blot analysis. Oroxylin A induced slow but sustained increases in intracellular calcium level and activated ERK1/2 mitogen activated protein kinase (MAPK). In addition, oroxylin A phosphorylated cyclic AMP response element binding protein (CREB) at Ser 133 in concentration and time dependent manner. Pretreatment with the MAPK inhibitor PD98059 (10μM) attenuated phosphorylation of ERK1/2 and CREB as well as BDNF production, which suggests that oroxylin A regulates BDNF production by activating MAPK-CREB pathway. GABA(A) antagonist bicuculline mimicked the effects of oroxylin A on BDNF production as well as MAPK-CREB pathway. Increase in intracellular Ca(2+) concentration, phosphorylation of ERK1/2 and CREB, and BDNF expression by oroxylin A was blocked by NMDA receptor inhibitor MK-801 (10μM) as well as tetrodotoxin (TTX, 0.5 and 1μM). The results from the present study suggest that the calcium and p-CREB dependent induction of BDNF expression, possibly via activation of synaptic NMDA receptor through the blockade of GABA(A) activity in cortical neuronal circuitry, might be responsible for the neuroprotective or memory enhancing effects of oroxylin A.

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' class='bbc_url' title='External link' rel='nofollow external'>http://ep.physoc.org/content/early/2009/09/09/expphysiol.2009.048561']ROLE OF EXERCISE-INDUCED BDNF PRODUCTION IN THE REGULATION OF ENERGY HOMEOSTASIS
Bente Klarlund Pedersen1,3, Maria Pedersen1, Karen S. Krabbe1, Helle Bruunsgaard1, Vance B. Matthews2 and Mark A. Febbraio2
+ Author Affiliations
1 University of Copenhagen;
2 Baker Heart Research Institute
* Corresponding author; email: bkp@rh.dk
Abstract
Brain derived neurotrophic factor (BDNF) has been shown to regulate neuronal development and plasticity and plays a role in learning and memory. Moreover, it is well-established that BDNF plays a role in the hypothalamic pathway that controls body weight and energy homeostasis. Recent evidence identifies BDNF as a player not only in central metabolism, but also in regulating energy metabolism in peripheral organs. Low levels of BDNF are found in patients with neurodegenerative diseases, including Alzheimer's disease and major depression. In addition, BDNF levels are low in obesity and independently so in patients with type 2 diabetes. BDNF is expressed in non-neurogenic tissues, including skeletal muscle and exercise increases BDNF levels not only in the brain and in plasma, but in skeletal muscle as well. BDNF mRNA and protein expression was increased in muscle cells that were electrically stimulated and BDNF increased phosphorylation of AMPK and ACCbeta and enhanced fatty oxidation both in vitro and ex vivo. These data identify BDNF as a contraction-inducible protein in skeletal muscle that is capable of enhancing lipid oxidation in skeletal muscle via activation of AMPK. Thus, BDNF appears to play a role both in neurobiology and in central as well as peripheral metabolism. The finding of low BDNF levels in both neurodegenerative diseases and in type 2 diabetes may explain the clustering of these diseases. BDNF is likely to mediate some of the beneficial effects of exercise with regard to protection against dementia and type 2 diabetes.

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Flavone:
' class='bbc_url' title='External link' rel='nofollow external'>http://www.pnas.org/content/107/6/2687.full']A selective TrkB agonist with potent neurotrophic activities by 7,8-dihydroxyflavone
Sung-Wuk Jang a , Xia Liu a , Manuel Yepes b , Kennie R. Shepherd c , Gary W. Miller c , Yang Liu d , W. David Wilson d , Ge Xiao e , Bruno Blanchi f , Yi E. Sun f , and Keqiang Ye a , 1
+ Author Affiliations
a Department of Pathology and Laboratory Medicine and
b Department of Neurology, Emory University School of Medicine, Atlanta, GA 30322;
c Department of Environmental and Occupational Health, Rollins Public School of Health, Emory University, Atlanta, GA 30322;
d Department of Chemistry, Georgia State University, Atlanta, GA 30302;
e Centers for Disease Control and Prevention, Atlanta, GA 30322; and
fNeuropsychiatric Institute, Medical Retardation Research Center, University of California, Los Angeles, Los Angeles, CA 90095
Edited* by Solomon Snyder, Johns Hopkins University School of Medicine, Baltimore, MD, and approved December 30, 2009 (received for review November 25, 2009)

Abstract
Brain-derived neurotrophic factor (BDNF), a cognate ligand for the tyrosine kinase receptor B (TrkB) receptor, mediates neuronal survival, differentiation, synaptic plasticity, and neurogenesis. However, BDNF has a poor pharmacokinetic profile that limits its therapeutic potential. Here we report the identification of 7,8-dihydroxyflavone as a bioactive high-affinity TrkB agonist that provokes receptor dimerization and autophosphorylation and activation of downstream signaling. 7,8-Dihydroxyflavone protected wild-type, but not TrkB-deficient, neurons from apoptosis. Administration of 7,8-dihydroxyflavone to mice activated TrkB in the brain, inhibited kainic acid-induced toxicity, decreased infarct volumes in stroke in a TrkB-dependent manner, and was neuroprotective in an animal model of Parkinson disease. Thus, 7,8-dihydroxyflavone imitates BDNF and acts as a robust TrkB agonist, providing a powerful therapeutic tool for the treatment of various neurological diseases.

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Glycoside:
' class='bbc_url' title='External link' rel='nofollow external'>http://www.ncbi.nlm.nih.gov/pubmed/20176057']Long-term treatment with peony glycosides reverses chronic unpredictable mild stress-induced depressive-like behavior via increasing expression of neurotrophins in rat brain.
Mao QQ, Xian YF, Ip SP, Tsai SH, Che CT.
Source
School of Chinese Medicine, The Chinese University of Hong Kong, Shatin, NT, Hong Kong, China.
Abstract
The root part of Paeonia lactiflora Pall., commonly known as peony, is a commonly used Chinese herb for the treatment of depression-like disorders. Previous studies in our laboratory have showed that total glycosides of peony (TGP) produced antidepressant-like action in various mouse models of behavioral despair. The present study aimed to investigate the mechanism(s) underlying the antidepressant-like action of TGP by measuring neurotrophins including brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) in non-stressed and chronic unpredictable mild stress (CUMS)-treated rats. TGP (80 or 160 mg/kg/day) was administered by oral gavage to the animals for 5 weeks. The results showed that CUMS caused depression-like behavior in rats, as indicated by the significant decreases in sucrose consumption and locomotor activity (assessed by open-field test). In addition, it was found that BDNF contents in the hippocampus and frontal cortex were significantly decreased in CUMS-treated rats. CUMS treatment also significantly decreased the level of NGF in the frontal cortex of the animals. Daily intragastric administration of TGP (80 or 160 mg/kg/day) during the five weeks of CUMS significantly suppressed behavioral and biochemical changes induced by CUMS. Treating non-stressed animals with TGP (160 mg/kg) for 5 weeks also significantly increased BDNF contents in the hippocampus and frontal cortex, and NGF contents in the frontal cortex. The results suggest that the antidepressant-like action of TGP is mediated, at least in part, by increasing the expression of BDNF and NGF in selective brain tissues.

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#88 Soma

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Posted 19 July 2012 - 07:22 PM

Preventing Suicide by Increasing BDNF

Ongoing research in neuroscience is demonstrating that meaning in life is deeply connected to the condition of the brain. Whether people judge their lives as meaningful or not is determined by neurotransmitters and brain activity in response to genetic and environmental influences. This indicates that a sense of meaning in life is associated with certain biological states. Finding the right biological influences could help a person feel like his or her life is meaningful and valuable.

Multiple studies show that hopelessness is associated with suicidal behavior (Link 1, Link 2, Link 3, Link 4, Link 5, Link 6) and this is barely the tip of the research on hopelessness and suicide, although a recent study indicates insomnia may be an even stronger predictor of suicidal behavior (Link). Psychology and psychiatry have devoted great effort to predicting human behavior in a variety of areas. Developing better ways to predict and prevent suicide is an important mission.

Some of the most fascinating and useful lessons on preventing and treating depression come from postmortem studies of suicide victims. A study that conducted brain autopsies on people who committed suicide and compared their brains to a control group discovered some interesting findings. The study found reduced messenger RNA levels of BDNF and trk B in the prefrontal cortex and hippocampus in the brains of people who committed suicide. Another study replicated the reduced BDNF in the hippocampus and prefrontal cortex of suicide victims. Multiple studies (Link 1, Link 2, Link 3, Link 4, Link 5) show that low levels of BDNF are found in patients with depression, anxiety, and/or bipolar disorder.

Since these results were first published, elevating BDNF levels in certain parts of the brain has become a promising area of research. Vigorous exercise improves mood in depressed patients and is recommended in many books and articles about natural treatments for depression. In fact, a study shows that intense exercise raises BDNF levels. Exercise also helps normalize BDNF in patients with panic disorder (Link). Some other studies show the involvement of BDNF in treating depression. Some of these studies involve animal models of depression, but they are still useful for identifying therapies that raise BDNF and could potentially be tested in humans.

Medications:

1. Ketamine use, which has rapid antidepressant properties, is associated with elevated levels of BDNF. (Link)

2. Memantine, which has antidepressant properties, elevates levels of BDNF. (Link)

3. Agomelatine increases hippocampal BDNF and has antidepressant properties. (Link)

4. Riluzole restores hippocampal BDNF expression and has antidepressant properties. (Link)

5. Escitalopram is an antidepressant that reverses BDNF deficits. (Link)

6. Atypical antipsychotics increase BDNF levels and have antidepressant effects. (Link)

7. Venlafaxine is an antidepressant that increases BDNF levels. (Link)

8. Olanzapine increases BDNF levels and augments antidepressant treatment. (Link)

9. Lithium upregulates BDNF and treats bipolar disorder. (Link)

10. Sertraline is an antidepressant that increases BDNF. (Link)

11. Risperidone increases BDNF levels and augments antidepressant treatment. (Link)

12. Imipramine is an antidepressant that up-regulates BDNF expression. (Link)

13. Mirtazapine is an antidepressant that increases BDNF gene expression. (Link)

14. Metyrapone enhances BDNF gene expression and has antidepressant properties. (Link)

15. Rolipram normalizes BDNF levels and has antidepressant properties. (Link)

Other Psychiatric Treatments:

1. Repetitive transcranial magnetic stimulation increases BDNF levels and has antidepressant effects. (Link)

2. Electroconvulsive therapy elevates BDNF levels and has antidepressant effects. (Link)

3. Vagal nerve stimulation activates BDNF receptors and treats depression. (Link)

Food and Lifestyle:

1. A Mediterranean diet increases BDNF levels in depressed patients. (Link)

2. Green odor elevates BDNF and has antidepressant properties. (Link)

3. Music enhances BDNF levels and improves mood. (Link)

4. Alpha-linolenic acid increases BDNF and reduces depressive behavior. (Link)

Supplements:

1. Fish oil has antidepressant effects that involve BDNF. (Link)

2. Ginsenoside prevents a stress-induced reduction in BDNF levels. (Link)

3. Hyperoside has antidepressant properties and elevates BDNF expression. (Link)

4. Magnolol restores BDNF expression and has antidepressant effects. (Link)

5. Curcumin reverses a decrease in BDNF levels and produces an antidepressant effect. (Link)

6. Zinc increases the BDNF mRNA level and has antidepressant effects. (Link)

7. Beta-alanine increases BDNF concentration and has anti-anxiety properties. (Link)

8. Flavonols enhance BDNF expression and have antidepressant properties. (Link)

9. Suyu-Jiaonang attenuates a reduction in BDNF and has antidepressant properties. (Link)

10. Ferulic acid increases BDNF mRNA and ameliorates stress-induced depressive behavior. (Link)

11. Nicotine increases BDNF levels and has antidepressant properties. (Link)

12. Polygala tenuifolia increases BDNF expression and has antidepressant effects. (Link)

13. Xiaoyaosan reverses decreases in BDNF and has antidepressant effects. (Link)

14. Piperine reverses the reduction in BDNF and has antidepressant properties. (Link)

15. Danzhi Xiaoyao powder increases BDNF levels and reduces depressive symptoms. (Link)

16. Ginkgo biloba extract increases BDNF expression and reduces the effects of stress. (Link)

17. Eugenol has antidepressant activity and induces BDNF. (Link)

Happiness and meaning in life are inseparable from biological traits. Understanding this fact opens up fascinating areas of research in preventing suicide. This is not the last word in suicide prevention. The next two posts will explore more research into neurological and genetic causes of suicide.

http://samsnyder.com...ncreasing-bdnf/


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#89 Soma

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Posted 19 July 2012 - 07:26 PM


Extract from Terminalia chebula seeds protect against experimental ischemic neuronal damage via maintaining SODs and BDNF levels.
Park JH, Joo HS, Yoo KY, Shin BN, Kim IH, Lee CH, Choi JH, Byun K, Lee B, Lim SS, Kim MJ, Won MH.
Source
Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon 200-701, South Korea.
Abstract
The fruit of Terminalia chebula Retz has been used as a traditional medicine in Asia and contains tannic acid, chebulagic acid, chebulinic acid and corilagin. Extract from T. chebula seeds (TCE) has various biological functions. We observed the neuroprotective effects of TCE against ischemic damage in the hippocampal C1 region (CA1) of the gerbil that had received oral administrations of TCE (100 mg/kg) once a day for 7 days before the induction of transient cerebral ischemia. In the TCE-treated ischemia group, neuronal neuclei (a marker for neurons)-positive neurons were distinctively abundant (62% of the sham group) in the CA1 4 days after ischemia-reperfusion (I-R) compared to those (12.2% of the sham group) in the vehicle-treated ischemia group. Four days after I-R TCE treatment markedly decreased the activation of astrocytes and microglia in the ischemic CA1 compared with the vehicle-treated ischemia group. In addition, immunoreactivities of Cu, Zn-superoxide dismutase (SOD1), Mn-superoxide dismutase (SOD2) and brain-derived neurotrophic factor (BDNF) in the CA1 of the TCE-treated ischemia group were much higher than those in the vehicle-ischemia group 4 days after I-R. Protein levels of SOD1, SOD2 and BDNF in the TCE-treated ischemia group were also much higher than those in the vehicle-ischemia group 4 days after I-R. These results indicate that the repeated supplement of TCE protected neurons from ischemic damage induced by transient cerebral ischemia by maintaining SODs and BDNF levels as well as decreasing glial activation.


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#90 golden1

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Posted 19 July 2012 - 08:51 PM

Honestly,

7,8-dihydroxyflavone looked really interesting from the abstract... and I feel like it shouldn't be that hard to get in bulk considering it's a flavonoid and common in plants.


http://pubs.acs.org/....1021/jm101206p
also:

We have successfully identified 4′-dimethylamino-7,8-dihydroxyflavone that displays higher TrkB agonistic activity than that of the lead. This novel compound also exhibits a more robust and longer TrkB activation effect in animals. Consequently, this new compound reveals more potent antiapoptotic activity. Interestingly, chronic oral administration of 4′-dimethylamino-7,8-dihydroxyflavone and its lead strongly promotes neurogenesis in dentate gyrus and demonstrates marked antidepressant effects. Hence, our data support that the synthetic 4′-dimethylamino-7,8-dihydroxyflavone and its lead both are orally bioavailable TrkB agonists and possess potent antidepressant effects.


A more potent synthetic analog...





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