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KoolK3n
post Mar 28, 2012, 05:51 AM
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Many people on Longecity believe Noopept has 1000x the potency of Piracetam. What other evidence exists besides the one reference on wikipedia from Russian scientists?

Here:
http://en.wikipedia.org/wiki/Noopept#cite_...-pmid12596521-2
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GodConsciousness
post Mar 28, 2012, 06:41 AM
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QUOTE(KoolK3n @ Mar 28, 2012, 09:51 AM) *

Many people on Longevity believe Noopept has 1000x the potency of Piracetam. What other evidence exists besides the one reference on wikipedia from Russian scientists?

Here:
http://en.wikipedia.org/wiki/Noopept#cite_...-pmid12596521-2


J Mol Biol. 2011 Dec 16;414(5):699-712. Epub 2011 Oct 1.
Neuroprotective and nootropic drug noopept rescues α-synuclein amyloid cytotoxicity.
Jia X, Gharibyan AL, ÷hman A, Liu Y, Olofsson A, Morozova-Roche LA.
Source
Department of Medical Biochemistry and Biophysics, UmeŚ University, SE-90187 UmeŚ, Sweden.
Abstract
Parkinson's disease is a common neurodegenerative disorder characterized by α-synuclein (α-Syn)-containing Lewy body formation and selective loss of dopaminergic neurons in the substantia nigra. We have demonstrated the modulating effect of noopept, a novel proline-containing dipeptide drug with nootropic and neuroprotective properties, on α-Syn oligomerization and fibrillation by using thioflavin T fluorescence, far-UV CD, and atomic force microscopy techniques. Noopept does not bind to a sterically specific site in the α-Syn molecule as revealed by heteronuclear two-dimensional NMR analysis, but due to hydrophobic interactions with toxic amyloid oligomers, it prompts their rapid sequestration into larger fibrillar amyloid aggregates. Consequently, this process rescues the cytotoxic effect of amyloid oligomers on neuroblastoma SH-SY5Y cells as demonstrated by using cell viability assays and fluorescent staining of apoptotic and necrotic cells and by assessing the level of intracellular oxidative stress. The mitigating effect of noopept against amyloid oligomeric cytotoxicity may offer additional benefits to the already well-established therapeutic functions of this new pharmaceutical.
Copyright © 2011 Elsevier Ltd. All rights reserved.
PMID: 21986202 [PubMed - indexed for MEDLINE]

Eksp Klin Farmakol. 2010 Dec;73(12):2-5.
[On the mechanism of noopept action: decrease in activity of stress-induced kinases and increase in expression of neutrophines].
[Article in Russian]
Ostrovskaia RU, Vakhitova IuV, Salimgareeva MKh, Iamidanov RS, Sadovnikov SV, Kapitsa IG, Seredenin SB.
Abstract
The influence of noopept (N-phenylacetyl-L-prolylglycine ethyl ester, GVS-111)--a drug combining the nootrope and neuroprotector properties--on the activity of mitogen-activated protein kinases (MAPKs) and the level of NGF and BDNF gene and protein expression in the frontal cortex, hippocampus, and hypothalamus has been studied in rats. Under conditions of chronic administration (28 days, 0.5 mg/day, i.p.), noopept decreased the activity of stress-induced kinases (SAPK/JNK 46/54 and pERK1/2) in rat hippocampus and increases the level of mRNA of the BDNF gene in both hypothalamus and hippocampus. The content of BDNF protein in the hypothalamus was also somewhat increased. In the context of notions about the activation of stress-induced kinases, as an important factor of amyloidogenesis and tau-protein deposition in brain tissue, and the role of deficiency of the neurotrophic factors in the development of neurodegenerative processes, the observed decrease in the activity of stress-activated MAPKs and increased expression of BDNF as a result of noopept administration suggest thatthis drug hasaspecific activity withrespect to some pathogenetic mechanisms involved in the Alzheimer disease.
PMID: 21395007 [PubMed - indexed for MEDLINE]


Neurosci Lett. 2010 May 31;476(2):70-3. Epub 2010 Apr 9.
Novel nootropic dipeptide Noopept increases inhibitory synaptic transmission in CA1 pyramidal cells.
Kondratenko RV, Derevyagin VI, Skrebitsky VG.
Source
Department of Brain Research, Scientific Center of Neurology, Russian Academy of Medical Sciences, by-str. Obukha 5, Moscow 105064, Russia.
Abstract
Effects of newly synthesized nootropic and anxiolytic dipeptide Noopept on inhibitory synaptic transmission in hippocampal CA1 pyramidal cells were investigated using patch-clamp technique in whole-cell configuration. Bath application of Noopept (1 microM) significantly increased the frequency of spike-dependant spontaneous IPSCs whereas spike-independent mIPSCs remained unchanged. It was suggested that Noopept mediates its effect due to the activation of inhibitory interneurons terminating on CA1 pyramidal cells. Results of current clamp recording of inhibitory interneurons residing in stratum radiatum confirmed this suggestion.
Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
PMID: 20382202 [PubMed - indexed for MEDLINE]

Eksp Klin Farmakol. 2010 Jan;73(1):2-6.
[Effect of the novel nootropic and neuroprotective dipeptide noopept on the streptozotocin-induced model of sporadic Alzheimer disease in rats].
[Article in Russian]
Ostrovskaia RU, Tsaplina AP, Vakhitova IuV, Salimgareeva MKh, Iamidanov RS.
Abstract
Streptozotocin-intracerebroventricularly treated rats are proposed as an experimental model of sporadic Alzheimer disease (AD). Diabetogenic toxin streptozotocin (STZ) administered in both cerebral ventricles in a dose of 3 mg/kg decreases the expression of NGF and BDNF mainly in the hippocampus and increases the content of malonic dialdehyde (MDA)--a product of lipid peroxidation--in the brain tissues. These metabolic changes are accompanied by a pronounced cognitive deficiency, which is manifested by long-term memory deterioration in the passive avoidance test. These manifestations of pathology are not accompanied by hyperglycemia in the case of intraventricular STZ administration, in contrast to the systemic (in particular, intraperitoneal) route of introduction that causes a pronounced increase in the blood glucose level. These results are consistent with the existing notions that (i) STZ administered intraventricularly provokes a complex of changes imitating the sporadic AD and (ii) this disease can be considered as a manifestation of type-III diabetes. The new original cognition enhancing and neuroprotective dipeptide noopept decreases the aforementioned metabolic changes and the accompanying long-term deterioration of the memory. Previously, this systemically active dipeptide was shown to be capable of increasing expression of NGF and BDNF in the hippocampus, stimulating the antibody production to beta-amyloid, inhibiting the lipid peroxidation, activating the endogenous antioxidant systems, and decreasing the rate of glutamate release (cholinopositive effect). Taken together, these data indicate that noopept can be considered as a multipotent substance acting upon several important pathogenic chainsof the sporadic AD.
PMID: 20184279 [PubMed - indexed for MEDLINE]
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KoolK3n
post Mar 28, 2012, 07:19 AM
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QUOTE(GodConsciousness @ Mar 28, 2012, 09:41 AM) *

J Mol Biol. 2011 Dec 16;414(5):699-712. Epub 2011 Oct 1.
Neuroprotective and nootropic drug noopept rescues α-synuclein amyloid cytotoxicity.
Jia X, Gharibyan AL, ÷hman A, Liu Y, Olofsson A, Morozova-Roche LA.
Source
Department of Medical Biochemistry and Biophysics, UmeŚ University, SE-90187 UmeŚ, Sweden.
Abstract
Parkinson's disease is a common neurodegenerative disorder characterized by α-synuclein (α-Syn)-containing Lewy body formation and selective loss of dopaminergic neurons in the substantia nigra. We have demonstrated the modulating effect of noopept, a novel proline-containing dipeptide drug with nootropic and neuroprotective properties, on α-Syn oligomerization and fibrillation by using thioflavin T fluorescence, far-UV CD, and atomic force microscopy techniques. Noopept does not bind to a sterically specific site in the α-Syn molecule as revealed by heteronuclear two-dimensional NMR analysis, but due to hydrophobic interactions with toxic amyloid oligomers, it prompts their rapid sequestration into larger fibrillar amyloid aggregates. Consequently, this process rescues the cytotoxic effect of amyloid oligomers on neuroblastoma SH-SY5Y cells as demonstrated by using cell viability assays and fluorescent staining of apoptotic and necrotic cells and by assessing the level of intracellular oxidative stress. The mitigating effect of noopept against amyloid oligomeric cytotoxicity may offer additional benefits to the already well-established therapeutic functions of this new pharmaceutical.
Copyright © 2011 Elsevier Ltd. All rights reserved.
PMID: 21986202 [PubMed - indexed for MEDLINE]

Eksp Klin Farmakol. 2010 Dec;73(12):2-5.
[On the mechanism of noopept action: decrease in activity of stress-induced kinases and increase in expression of neutrophines].
[Article in Russian]
Ostrovskaia RU, Vakhitova IuV, Salimgareeva MKh, Iamidanov RS, Sadovnikov SV, Kapitsa IG, Seredenin SB.
Abstract
The influence of noopept (N-phenylacetyl-L-prolylglycine ethyl ester, GVS-111)--a drug combining the nootrope and neuroprotector properties--on the activity of mitogen-activated protein kinases (MAPKs) and the level of NGF and BDNF gene and protein expression in the frontal cortex, hippocampus, and hypothalamus has been studied in rats. Under conditions of chronic administration (28 days, 0.5 mg/day, i.p.), noopept decreased the activity of stress-induced kinases (SAPK/JNK 46/54 and pERK1/2) in rat hippocampus and increases the level of mRNA of the BDNF gene in both hypothalamus and hippocampus. The content of BDNF protein in the hypothalamus was also somewhat increased. In the context of notions about the activation of stress-induced kinases, as an important factor of amyloidogenesis and tau-protein deposition in brain tissue, and the role of deficiency of the neurotrophic factors in the development of neurodegenerative processes, the observed decrease in the activity of stress-activated MAPKs and increased expression of BDNF as a result of noopept administration suggest thatthis drug hasaspecific activity withrespect to some pathogenetic mechanisms involved in the Alzheimer disease.
PMID: 21395007 [PubMed - indexed for MEDLINE]


Neurosci Lett. 2010 May 31;476(2):70-3. Epub 2010 Apr 9.
Novel nootropic dipeptide Noopept increases inhibitory synaptic transmission in CA1 pyramidal cells.
Kondratenko RV, Derevyagin VI, Skrebitsky VG.
Source
Department of Brain Research, Scientific Center of Neurology, Russian Academy of Medical Sciences, by-str. Obukha 5, Moscow 105064, Russia.
Abstract
Effects of newly synthesized nootropic and anxiolytic dipeptide Noopept on inhibitory synaptic transmission in hippocampal CA1 pyramidal cells were investigated using patch-clamp technique in whole-cell configuration. Bath application of Noopept (1 microM) significantly increased the frequency of spike-dependant spontaneous IPSCs whereas spike-independent mIPSCs remained unchanged. It was suggested that Noopept mediates its effect due to the activation of inhibitory interneurons terminating on CA1 pyramidal cells. Results of current clamp recording of inhibitory interneurons residing in stratum radiatum confirmed this suggestion.
Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
PMID: 20382202 [PubMed - indexed for MEDLINE]

Eksp Klin Farmakol. 2010 Jan;73(1):2-6.
[Effect of the novel nootropic and neuroprotective dipeptide noopept on the streptozotocin-induced model of sporadic Alzheimer disease in rats].
[Article in Russian]
Ostrovskaia RU, Tsaplina AP, Vakhitova IuV, Salimgareeva MKh, Iamidanov RS.
Abstract
Streptozotocin-intracerebroventricularly treated rats are proposed as an experimental model of sporadic Alzheimer disease (AD). Diabetogenic toxin streptozotocin (STZ) administered in both cerebral ventricles in a dose of 3 mg/kg decreases the expression of NGF and BDNF mainly in the hippocampus and increases the content of malonic dialdehyde (MDA)--a product of lipid peroxidation--in the brain tissues. These metabolic changes are accompanied by a pronounced cognitive deficiency, which is manifested by long-term memory deterioration in the passive avoidance test. These manifestations of pathology are not accompanied by hyperglycemia in the case of intraventricular STZ administration, in contrast to the systemic (in particular, intraperitoneal) route of introduction that causes a pronounced increase in the blood glucose level. These results are consistent with the existing notions that (i) STZ administered intraventricularly provokes a complex of changes imitating the sporadic AD and (ii) this disease can be considered as a manifestation of type-III diabetes. The new original cognition enhancing and neuroprotective dipeptide noopept decreases the aforementioned metabolic changes and the accompanying long-term deterioration of the memory. Previously, this systemically active dipeptide was shown to be capable of increasing expression of NGF and BDNF in the hippocampus, stimulating the antibody production to beta-amyloid, inhibiting the lipid peroxidation, activating the endogenous antioxidant systems, and decreasing the rate of glutamate release (cholinopositive effect). Taken together, these data indicate that noopept can be considered as a multipotent substance acting upon several important pathogenic chainsof the sporadic AD.
PMID: 20184279 [PubMed - indexed for MEDLINE]


All of them are from Europe with three in Russian. My concern with Noopept wasn't it's cognitive enhancement but the possibility that the 1000x potency claim was over-exaggerated. Thank you for those abstracts!
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GodConsciousness
post Mar 28, 2012, 07:49 AM
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1,000 times stronger seems a bit high to me as well, but you do need much lower doses and noopept has different modes of action compared to piracetam.
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LeeCrostM.D.
post Jul 02, 2012, 05:54 AM
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QUOTE(KoolK3n @ Mar 28, 2012, 05:51 AM) *

Many people on Longecity believe Noopept has 1000x the potency of Piracetam. What other evidence exists besides the one reference on wikipedia from Russian scientists?

Here:
http://en.wikipedia.org/wiki/Noopept#cite_...-pmid12596521-2


Until I can review more human clinical research on it I do not recommend taking it. There are much better understood and clinically studied nootropics available.
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KoolK3n
post Jul 02, 2012, 06:14 AM
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QUOTE(LeeCrostM.D. @ Jul 02, 2012, 08:54 AM) *

QUOTE(KoolK3n @ Mar 28, 2012, 05:51 AM) *

Many people on Longecity believe Noopept has 1000x the potency of Piracetam. What other evidence exists besides the one reference on wikipedia from Russian scientists?

Here:
http://en.wikipedia.org/wiki/Noopept#cite_...-pmid12596521-2


Until I can review more human clinical research on it I do not recommend taking it. There are much better understood and clinically studied nootropics available.


Huperzine is not one of them
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neurofire
post Jul 23, 2012, 03:41 AM
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Hmm interesting, I have not looked into noopept before. I have had my eyes set on a similar nootropic that only seems to exist in Russia, Phenylpiracetam (phenotropyl). Aaaah why can't these be available in the US and not just hiding out in Russia!?

I do not recommend going by strength ratings alone. With the existing racetams, they are proclaimed to be "X times stronger than piracetam." I do not know how this 'strength' is estimated, but the effects of each are very different from one another, and that is really what makes the difference. I would recommend ordering some and trying it; that is the best evidence you will get!
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bzyzny
post Jan 22, 2013, 06:19 AM
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I believe it simply means that the effective dosage is 1000x, approximately, since the normal dosage of noopept is 10-30mg per day whereas the normal dosage of piracetam is 3-9g per day. It is not in reference to the effects of the substances, AFAIK. Although user reports do indicate that noopept is noticeably better or more effective than piracetam. Can anyone confirm or deny my assumption?
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globetrotter
post Feb 21, 2013, 02:20 PM
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@bzyzny - I just finished my 3 month trial with noopept. I initially (3 weeks) replaced my piracetam with noopept after a one week washout. Initial results were positive but subtle: elevated energy, good focus, pretty much par with piracetam. However, contrary to the wikipedia entry I noticed a marked increase in irritability towards others (specifically) and situations (in general). I also noticed jittery-ness after my 3rd 10mg dose of the day. After 3 weeks of using just noopept I opted to reintroduce piracetam in my stack. I think the two synergize well initially but the noopept seemed to "fade" after a while.

YMMV, but for me noopept won't be part of my regular rotation. I tossed the remainder...piracetam is so darn cheap and so well tolerated smile.gif
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Tone
post Mar 19, 2013, 09:29 PM
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Its an error. 10 is 1/100th of 1000, not 1/1000th. so 100 times potency
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Tone
post Mar 19, 2013, 09:31 PM
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wake me up when there is an AMPA NEGATIVE allosteric modulator thats cheap and easy to get. ; racetams are AMPA POSITIVE allosteric modulators.
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