- Feb 17, 2014
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Noopept helps to restore memory and cognitive functions, disturbed as a result of brain injury, ischemia, hypoxia, the effects of alcohol and other toxic substances.
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Noopept....experiences from a long term user
- Thread starter johnjuanb1
- Start date
- Feb 17, 2014
- 2,168
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Post from a noopept user...
"I’m convinced that Noopept is the best traditional nootropic drug available in terms of price and efficacy."
"I’m convinced that Noopept is the best traditional nootropic drug available in terms of price and efficacy."
- Feb 17, 2014
- 2,168
- 0
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Post from a Superior noopept user at another forum...
"A little update... I am doing noopet 2xd and so is my wife. I do believe its working for both. Enough for me to order 8 bottle before the bogo went off we will blow thru 2 bottles a month. It is g2g give you a good sense of well being and mind is sharper. I actually feel a little more comfortable talking to new people now."
"A little update... I am doing noopet 2xd and so is my wife. I do believe its working for both. Enough for me to order 8 bottle before the bogo went off we will blow thru 2 bottles a month. It is g2g give you a good sense of well being and mind is sharper. I actually feel a little more comfortable talking to new people now."
- Feb 17, 2014
- 2,168
- 0
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Comparative activity of proline-containing dipeptide noopept and inhibitor of dipeptidyl peptidase-4 sitagliptin in a rat model of developing diabetes.
AuthorsOstrovskaya RU, et al. Show all Journal
Bull Exp Biol Med. 2014 Jan;156(3):342-6. doi: 10.1007/s10517-014-2345-z. Epub 2014 Jan 15.
Affiliation
Abstract
Developing diabetes was modeled on adult male Wistar rats by repeated intraperitoneal injections of streptozotocin in a subdiabetogenic dose of 30 mg/kg for 3 days. Proline-containing dipeptide drug Noopept or a standard diabetic drug dipeptidyl peptidase-4 inhibitor sitagliptin was administered per os in a dose of 5 mg/kg before each injection of the toxin and then for 16 days after streptozotocin course. In active control group, spontaneously increase glucose level and reduced tolerance to glucose load (1000 mg/kg intraperitoneally) were observed on the next day after the third administration of toxin. Basal glucose level decreased by day 16, but glucose tolerance remained impaired. Noopept normalized the basal blood glucose level and tolerance to glucose load on the next day after administration of streptozotocin. The effect of Noopept persisted to the end of the experiment. At early terms of the experiment, sitagliptin was somewhat superior to Noopept by the effect on baseline glucose level, but was inferior by the influence on glucose tolerance.. By the end of the experiment, Noopept significantly (by 2 times) surpassed sitagliptin by its effect on glucose tolerance.
AuthorsOstrovskaya RU, et al. Show all Journal
Bull Exp Biol Med. 2014 Jan;156(3):342-6. doi: 10.1007/s10517-014-2345-z. Epub 2014 Jan 15.
Affiliation
Abstract
Developing diabetes was modeled on adult male Wistar rats by repeated intraperitoneal injections of streptozotocin in a subdiabetogenic dose of 30 mg/kg for 3 days. Proline-containing dipeptide drug Noopept or a standard diabetic drug dipeptidyl peptidase-4 inhibitor sitagliptin was administered per os in a dose of 5 mg/kg before each injection of the toxin and then for 16 days after streptozotocin course. In active control group, spontaneously increase glucose level and reduced tolerance to glucose load (1000 mg/kg intraperitoneally) were observed on the next day after the third administration of toxin. Basal glucose level decreased by day 16, but glucose tolerance remained impaired. Noopept normalized the basal blood glucose level and tolerance to glucose load on the next day after administration of streptozotocin. The effect of Noopept persisted to the end of the experiment. At early terms of the experiment, sitagliptin was somewhat superior to Noopept by the effect on baseline glucose level, but was inferior by the influence on glucose tolerance.. By the end of the experiment, Noopept significantly (by 2 times) surpassed sitagliptin by its effect on glucose tolerance.
- Feb 17, 2014
- 2,168
- 0
- 36
Post from a SuperiorPeptide customer...
"I'm 53 years old, I was starting to get nervous about my memory, losing Shit, trying to recall actors from a movie and drawing a blank. So I did some research and found Noopept. JJb a Rep for Superior and long term user, posted his thoughts and a few articles, Research Papers etc. Anyway started it 4 days ago, Skeptical as usual ,and this Shit actually works! I don't have total Recall but my memory ,mood and energy level are definitely better."
"I'm 53 years old, I was starting to get nervous about my memory, losing Shit, trying to recall actors from a movie and drawing a blank. So I did some research and found Noopept. JJb a Rep for Superior and long term user, posted his thoughts and a few articles, Research Papers etc. Anyway started it 4 days ago, Skeptical as usual ,and this Shit actually works! I don't have total Recall but my memory ,mood and energy level are definitely better."
- Feb 17, 2014
- 2,168
- 0
- 36
Neuroprotective effect of novel cognitive enhancer noopept on AD-related cellular model involves the attenuation of apoptosis and tau hyperphosphorylation.
AuthorsOstrovskaya RU, et al. Show all Journal
J Biomed Sci. 2014 Aug 6;21(1):74. [Epub ahead of print]
Affiliation
Abstract
BackgroundNoopept (N-phenyl-acetyl-L-prolylglycine ethyl ester) was constructed as a dipeptide analog of the standard cognition enhancer, piracetam. Our previous experiments have demonstrated the cognition restoring effect of noopept in several animal models of Alzheimer disease (AD). Noopept was also shown to prevent ionic disbalance, excitotoxicity, free radicals and pro-inflammatory cytokines accumulation, and neurotrophine deficit typical for different kinds of brain damages, including AD. In this study, we investigated the neuroprotective action of noopept on cellular model of AD, Aß25¿35-induced toxicity in PC12 cells and revealed the underlying mechanisms.ResultsThe neuroprotective effect of noopept (added to the medium at 10 ¿M concentration, 72 hours before ¿ß25¿35) was studied on ¿ß25¿35-induced injury (5 ¿M for 24 h) in PC12 cells. The ability of drug to protect the impairments of cell viability, calcium homeostasis, ROS level, mitochondrial function, tau phosphorylation and neurite outgrowth caused by ¿ß25¿35 were evaluated.Following the exposure of PC12 cells to ¿ß25¿35 an increase of the level of ROS, intracellular calcium, and tau phosphorylation at Ser396 were observed; these changes were accompanied by a decrease in cell viability and an increase of apoptosis. Noopept treatment before the amyloid-beta exposure improved PC12 cells viability, reduced the number of early and late apoptotic cells, the levels of intracellular reactive oxygen species and calcium and enhanced the mitochondrial membrane potential. In addition, pretreatment of PC12 cell with noopept significantly attenuated tau hyperphosphorylation at Ser396 and ameliorated the alterations of neurite outgrowth evoked by ¿ß25¿35.ConclusionsTaken together, these data provide evidence that novel cognitive enhancer noopept protects PC12 cell against deleterious actions of Aß through inhibiting the oxidative damage and calcium overload as well as suppressing the mitochondrial apoptotic pathway. Moreover, neuroprotective properties of noopept likely include its ability to decrease tau phosphorylation and to restore the altered morphology of PC12 cells. Therefore, this nootropic dipeptide is able to positively affect not only common pathogenic pathways but also disease-specific mechanisms underlying Aß-related pathology.
AuthorsOstrovskaya RU, et al. Show all Journal
J Biomed Sci. 2014 Aug 6;21(1):74. [Epub ahead of print]
Affiliation
Abstract
BackgroundNoopept (N-phenyl-acetyl-L-prolylglycine ethyl ester) was constructed as a dipeptide analog of the standard cognition enhancer, piracetam. Our previous experiments have demonstrated the cognition restoring effect of noopept in several animal models of Alzheimer disease (AD). Noopept was also shown to prevent ionic disbalance, excitotoxicity, free radicals and pro-inflammatory cytokines accumulation, and neurotrophine deficit typical for different kinds of brain damages, including AD. In this study, we investigated the neuroprotective action of noopept on cellular model of AD, Aß25¿35-induced toxicity in PC12 cells and revealed the underlying mechanisms.ResultsThe neuroprotective effect of noopept (added to the medium at 10 ¿M concentration, 72 hours before ¿ß25¿35) was studied on ¿ß25¿35-induced injury (5 ¿M for 24 h) in PC12 cells. The ability of drug to protect the impairments of cell viability, calcium homeostasis, ROS level, mitochondrial function, tau phosphorylation and neurite outgrowth caused by ¿ß25¿35 were evaluated.Following the exposure of PC12 cells to ¿ß25¿35 an increase of the level of ROS, intracellular calcium, and tau phosphorylation at Ser396 were observed; these changes were accompanied by a decrease in cell viability and an increase of apoptosis. Noopept treatment before the amyloid-beta exposure improved PC12 cells viability, reduced the number of early and late apoptotic cells, the levels of intracellular reactive oxygen species and calcium and enhanced the mitochondrial membrane potential. In addition, pretreatment of PC12 cell with noopept significantly attenuated tau hyperphosphorylation at Ser396 and ameliorated the alterations of neurite outgrowth evoked by ¿ß25¿35.ConclusionsTaken together, these data provide evidence that novel cognitive enhancer noopept protects PC12 cell against deleterious actions of Aß through inhibiting the oxidative damage and calcium overload as well as suppressing the mitochondrial apoptotic pathway. Moreover, neuroprotective properties of noopept likely include its ability to decrease tau phosphorylation and to restore the altered morphology of PC12 cells. Therefore, this nootropic dipeptide is able to positively affect not only common pathogenic pathways but also disease-specific mechanisms underlying Aß-related pathology.