The Experts below are selected from a list of 249 Experts worldwide ranked by ideXlab platform
Enrico Righetti - One of the best experts on this subject based on the ideXlab platform.
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Piracetam for acute ischemic stroke
Stroke, 2006Co-Authors: Graeme J. Hankey, Stefano Ricci, Maria Grazia Celani, Teresa Anna Cantisani, Enrico RighettiAbstract:Piracetam is a drug which has been marketed in several countries for many years as a “nootropic” agent (that is, a drug which has metabolic activity on human brain), and for the treatment of myoclonus. Recently, a Cochrane review has been published on efficacy of Piracetam on ameliorating language in aphasic stroke patients; the drug has been reconsidered for acute stroke treatment as well. The objective of this review was to assess the effects of Piracetam in acute presumed ischemic stroke. Randomized trials comparing Piracetam with control, with at least mortality reported and entry to the trial within ≈48 hours of stroke onset. Two reviewers (S.R., M.G.C.) extracted data and assessed trial quality, and this was checked by the other 2 …
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The Cochrane Library - Piracetam for Acute Ischemic Stroke
Stroke, 2006Co-Authors: Graeme J. Hankey, Stefano Ricci, Maria Grazia Celani, Teresa Anna Cantisani, Enrico RighettiAbstract:Piracetam is a drug which has been marketed in several countries for many years as a “nootropic” agent (that is, a drug which has metabolic activity on human brain), and for the treatment of myoclonus. Recently, a Cochrane review has been published on efficacy of Piracetam on ameliorating language in aphasic stroke patients; the drug has been reconsidered for acute stroke treatment as well. The objective of this review was to assess the effects of Piracetam in acute presumed ischemic stroke. Randomized trials comparing Piracetam with control, with at least mortality reported and entry to the trial within ≈48 hours of stroke onset. Two reviewers (S.R., M.G.C.) extracted data and assessed trial quality, and this was checked by the other 2 …
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Piracetam in acute stroke: a systematic review
Journal of neurology, 2000Co-Authors: Stefano Ricci, Maria Grazia Celani, Teresa Anna Cantisani, Enrico RighettiAbstract:We studied whether the administration of Piracetam in acute, presumed ischemic stroke affects case fatality and functional outcome. The Cochrane Stroke Group strategy was used to evaluate all randomized controlled trials of patients with presumed ischemic stroke examined within 48 h; death and (when available) functional outcome were used as end points. Three studies were included; the most recent one contributed more than 97% of the data. There were 501 patients treated with Piracetam and 501 controls. Piracetam was associated with a nonsignificant 31% increase in the odds of death (95% CI –5% to 81%). This result was due almost completely to the effect of the larger trial, which, however, reported that the difference in case fatality rate between Piracetam and control disappeared after correcting for the imbalance in stroke severity between the two groups. Data on functional outcome were available only for the largest study, and no difference was reported. Data obtained from the manufacturer suggested a nonsignificant trend (–10%) towards reduction in dependency with Piracetam (CI –33% to 20%); the proportions of patients dead or dependent in the two groups were the same. Relevant adverse effects were not reported. The evidence from this review does not support routine administration of Piracetam in patients with acute ischemic stroke; however, since a possible beneficial effect cannot completely be ruled out, further controlled trials are warranted.
Walter E. Müller - One of the best experts on this subject based on the ideXlab platform.
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improved mitochondrial function in brain aging and alzheimer disease the new mechanism of action of the old metabolic enhancer Piracetam
Frontiers in Neuroscience, 2010Co-Authors: Kristina Leuner, Christopher Kurz, G Guidetti, Jeanmarc Orgogozo, Walter E. MüllerAbstract:Piracetam, the prototype of the so-called nootropic drugs’ is used since many years in different countries to treat cognitive impairment in aging and dementia. Findings that Piracetam enhances fluidity of brain mitochondrial membranes led to the hypothesis that Piracetam might improve mitochondrial function, e.g. might enhance ATP synthesis. This assumption has recently been supported by a number of observations showing enhanced mitochondrial membrane potential (MMP), enhanced ATP production, and reduced sensitivity for apoptosis in a variety of cell and animal models for aging and Alzheimer disease (AD). As a specific consequence, substantial evidence for elevated neuronal plasticity as a specific effect of Piracetam has emerged. Taken together, these new findings can explain many of the therapeutic effects of Piracetam on cognition in aging and dementia as well as different situations of brain dysfunctions.
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the metabolic enhancer Piracetam ameliorates the impairment of mitochondrial function and neurite outgrowth induced by s amyloid peptide
British Journal of Pharmacology, 2010Co-Authors: Christopher Kurz, Anne Eckert, Kristina Leuner, I Ungerer, U Lipka, S Kirr, Tanja Schutt, Walter E. MüllerAbstract:Background and purpose: β-Amyloid peptide (Aβ) is implicated in the pathogenesis of Alzheimer's disease by initiating a cascade of events from mitochondrial dysfunction to neuronal death. The metabolic enhancer Piracetam has been shown to improve mitochondrial dysfunction following brain aging and experimentally induced oxidative stress. Experimental approach: We used cell lines (PC12 and HEK cells) and murine dissociated brain cells. The protective effects of Piracetam in vitro and ex vivo on Aβ-induced impairment of mitochondrial function (as mitochondrial membrane potential and ATP production), on secretion of soluble Aβ and on neurite outgrowth in PC12 cells were investigated. Key results: Piracetam improves mitochondrial function of PC12 cells and acutely dissociated brain cells from young NMRI mice following exposure to extracellular Aβ1-42. Similar protective effects against Aβ1-42 were observed in dissociated brain cells from aged NMRI mice, or mice transgenic for mutant human amyloid precursor protein (APP) treated with Piracetam for 14 days. Soluble Aβ load was markedly diminished in the brain of those animals after treatment with Piracetam. Aβ production by HEK cells stably transfected with mutant human APP was elevated by oxidative stress and this was reduced by Piracetam. Impairment of neuritogenesis is an important consequence of Aβ-induced mitochondrial dysfunction and Aβ-induced reduction of neurite growth in PC12 cells was substantially improved by Piracetam. Conclusion and implications: Our findings strongly support the concept of improving mitochondrial function as an approach to ameliorate the detrimental effects of Aβ on brain function. This article is commented on by Moncada, pp. 217–219 of this issue. To view this commentary visit http://dx.doi.org/10.1111/j.1476-5381.2010.00706.x and to view related papers by Pravdic et al. and Puerta et al. visit http://dx.doi.org/10.1111/j.1476-5381.2010.00698.x and http://dx.doi.org/10.1111/j.1476-5381.2010.00663.x
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Piracetam improves mitochondrial dysfunction following oxidative stress
British journal of pharmacology, 2006Co-Authors: Uta Keil, Isabel Scherping, Susanne Hauptmann, Katin Schuessel, Anne Eckert, Walter E. MüllerAbstract:1.--Mitochondrial dysfunction including decrease of mitochondrial membrane potential and reduced ATP production represents a common final pathway of many conditions associated with oxidative stress, for example, hypoxia, hypoglycemia, and aging. 2.--Since the cognition-improving effects of the standard nootropic Piracetam are usually more pronounced under such pathological conditions and young healthy animals usually benefit little by Piracetam, the effect of Piracetam on mitochondrial dysfunction following oxidative stress was investigated using PC12 cells and dissociated brain cells of animals treated with Piracetam. 3.--Piracetam treatment at concentrations between 100 and 1000 microM improved mitochondrial membrane potential and ATP production of PC12 cells following oxidative stress induced by sodium nitroprusside (SNP) and serum deprivation. Under conditions of mild serum deprivation, Piracetam (500 microM) induced a nearly complete recovery of mitochondrial membrane potential and ATP levels. Piracetam also reduced caspase 9 activity after SNP treatment. 4.--Piracetam treatment (100-500 mg kg(-1) daily) of mice was also associated with improved mitochondrial function in dissociated brain cells. Significant improvement was mainly seen in aged animals and only less in young animals. Moreover, the same treatment reduced antioxidant enzyme activities (superoxide dismutase, glutathione peroxidase, and glutathione reductase) in aged mouse brain only, which are elevated as an adaptive response to the increased oxidative stress with aging. 5.--In conclusion, therapeutically relevant in vitro and in vivo concentrations of Piracetam are able to improve mitochondrial dysfunction associated with oxidative stress and/or aging. Mitochondrial stabilization and protection might be an important mechanism to explain many of Piracetam's beneficial effects in elderly patients.
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Effects of Piracetam on membrane fluidity in the aged mouse, rat, and human brain.
Biochemical pharmacology, 1997Co-Authors: Walter E. Müller, Sabrina Koch, Klaus Scheuer, Rostock Angelika, Reni BartschAbstract:In vitro preincubation of brain membranes of aged mice with Piracetam (0.1-1.0 mmol/L) enhanced membrane fluidity, as indicated by decreased anisotropy of the membrane-bound fluorescence probe 1,6-diphenyl-1,3,5-hexatriene (DPH). Piracetam had similar in vitro effects on brain membranes of aged rats and humans, but it did not alter brain membrane fluidity in young mice. Chronic treatment of young and aged rats with Piracetam (300 mg/kg once daily) significantly increased membrane fluidity in some brain regions of the aged animals, but had no measurable effect on membrane fluidity in the young rats. The same treatment significantly improved active avoidance learning in the aged rats only. It is suggested that some of the pharmacological properties of Piracetam can be explained by its effects on membrane fluidity.
Tom Leyssens - One of the best experts on this subject based on the ideXlab platform.
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crystallizing ionic cocrystals structural characteristics thermal behavior and crystallization development of a Piracetam cacl2 cocrystallization process
Crystal Growth & Design, 2018Co-Authors: Lixing Song, Koen Robeyns, Tom LeyssensAbstract:In this study, we aim to develop a robust crystallization process for the ionic cocrystal between Piracetam and CaCl2. We discuss the structural characteristics of the Piracetam-CaCl2 cocrystal and its thermal behavior; furthermore, we develop a robust crystallization process by construction of appropriate phase diagrams. CaCl2 and Piracetam form an ionic dihydrate cocrystal with formula Piracetam2·CaCl2·2H2O, in which the Ca2+ cation adopts an octahedral coordination with the oxygens of four different molecules of Piracetam and of two water molecules. According to the TGA, DSC, and VT-XRPD, the cocrystal exhibits improved thermal stability compared to the parent drug compound. In this article we show how one can develop a robust, water-based cocrystallization process for ionic cocrystals, a relatively underexplored part of the cocrystal landscape. We also discuss the common ion effect on cocrystallization, and show how a common ion can strongly impact on the solubility of the cocrystal, as well as its co...
Sarika Singh - One of the best experts on this subject based on the ideXlab platform.
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metabolic enhancer Piracetam attenuates the translocation of mitochondrion specific proteins of caspase independent pathway poly adp ribose polymerase 1 up regulation and oxidative dna fragmentation
Neurotoxicity Research, 2018Co-Authors: Dinesh Kumar Verma, Sonam Gupta, Joyshree Biswas, Neeraj Joshi, Sivarama K Raju, Mu Wahajuddin, Sarika SinghAbstract:Piracetam, a nootropic drug, has been clinically used for decades; however, its mechanism of action still remains enigmatic. The present study was undertaken to evaluate the role of mitochondrion-specific factors of caspase-independent pathway like apoptotic-inducing factor (AIF) and endonuclease-G (endo-G) in Piracetam-induced neuroprotection. N2A cells treated with lipopolysaccharide (LPS) exhibited significant cytotoxicity, impaired mitochondrial activity, and reactive oxygen species generation which was significantly attenuated with Piracetam co-treatment. Cells co-treated with LPS and Piracetam exhibited significant uptake of Piracetam in comparison to only Piracetam-treated cells as estimated by liquid chromatography-mass spectrometry (LC-MSMS). LPS treatment caused significant translocation of AIF and endonuclease-G in neuronal N2A cells which were significantly attenuated with Piracetam co-treatment. Significant over-expression of proinflammatory cytokines was also observed after treatment of LPS to cells which was inhibited with Piracetam co-treatment demonstrating its anti-inflammatory property. LPS-treated cells exhibited significant oxidative DNA fragmentation and poly [ADP-ribose] polymerase-1 (PARP-1) up-regulation in nucleus, both of which were attenuated with Piracetam treatment. Antioxidant melatonin but not z-VAD offered the inhibited LPS-induced DNA fragmentation indicating the involvement of oxidative DNA fragmentation. Further, we did not observe the altered caspase-3 level after LPS treatment initially while at a later time point, significantly augmented level of caspase-3 was observed which was not inhibited with Piracetam treatment. In total, our findings indicate the interference of Piracetam in mitochondrion-mediated caspase-independent pathway, as well as its anti-inflammatory and antioxidative properties. Graphical Abstract Graphical abstract indicating the novel interference of metabolic enhancer Piracetam (P) in neuronal death mechanisms.
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metabolic enhancer Piracetam attenuates rotenone induced oxidative stress a study in different rat brain regions
Acta Neurobiologiae Experimentalis, 2015Co-Authors: Dinesh Kumar Verma, Neeraj Joshi, Kunumuri Sivarama Raju, Muhammad Wahajuddin, R K Singh, Sarika SinghAbstract:Piracetam is clinically being used nootropic drug but the details of its neuroprotective mechanism are not well studied. The present study was conducted to assess the effects of Piracetam on rotenone induced oxidative stress by using both ex vivo and in vivo test systems. Rats were treated with Piracetam (600 mg/kg b.w. oral) for seven constitutive days prior to rotenone administration (intracerebroventricular, 12 µg) in rat brain. Rotenone induced oxidative stress was assessed after 1 h and 24 h of rotenone administration. Ex vivo estimations were performed by using two experimental designs. In one experimental design the rat brain homogenate was treated with rotenone (1 mM, 2 mM and 4 mM) and rotenone+Piracetam (10 mM) for 1 h. While in second experimental design the rats were pretreated with Piracetam for seven consecutive days. On eighth day the rats were sacrificed, brain homogenate was prepared and treated with rotenone (1 mM, 2 mM and 4mM) for 1h. After treatment the glutathione (GSH) and malondialdehyde (MDA) levels were estimated in brain homogenate. In vivo study showed that pretreatment of Piracetam offered significant protection against rotenone induced decreased GSH and increased MDA level though the protection was region specific. But the co-treatment of Piracetam with rotenone did not offer significant protection against rotenone induced oxidative stress in ex vivo study. Whereas ex vivo experiments in rat brain homogenate of Piracetam pretreated rats, showed the significant protection against rotenone induced oxidative stress. Findings indicated that pretreatment of Piracetam significantly attenuated the rotenone induced oxidative stress though the protection was region specific. Piracetam treatment to rats led to its absorption and accumulation in different brain regions as assessed by liquid chromatography mass spectrometry/mass spectrometry. In conclusion, study indicates the Piracetam is able to enhance the antioxidant capacity in brain cells in region specific manner. The study is also revealing the rationale for its clinical use in cognitive impairment and other neurological diseases.
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The metabolic enhancer Piracetam attenuates mitochondrion-specific endonuclease G translocation and oxidative DNA fragmentation.
Free radical biology & medicine, 2014Co-Authors: Sonam Gupta, Dinesh Kumar Verma, Joyshree Biswas, K. Siva Rama Raju, Neeraj Joshi, Wahajuddin, Sarika SinghAbstract:This study was performed to investigate the involvement of mitochondrion-specific endonuclease G in Piracetam (P)-induced protective mechanisms. Studies have shown the antiapoptotic effects of Piracetam but the mechanism of action of Piracetam is still an enigma. To assess the involvement of endonuclease G in Piracetam-induced protective effects, astrocyte glial cells were treated with lipopolysaccharide (LPS) and Piracetam. LPS treatment caused significantly decreased viability, mitochondrial activity, oxidative stress, chromatin condensation, and DNA fragmentation, which were attenuated by Piracetam cotreatment. Cotreatment of astrocytes with Piracetam showed its significantly time-dependent absorption as observed with high-performance liquid chromatography. Astrocytes treated with Piracetam alone showed enhanced mitochondrial membrane potential (MMP) in comparison to control astrocytes. However, in LPS-treated cells no significant alteration in MMP was observed in comparison to control cells. Protein and mRNA levels of the terminal executor of the caspase-mediated pathway, caspase-3, were not altered significantly in LPS or LPS + Piracetam-treated astrocytes, whereas endonuclease G was significantly translocated to the nucleus in LPS-treated astrocytes. Piracetam cotreatment attenuated the LPS-induced endonuclease G translocation. In conclusion this study indicates that LPS treatment of astrocytes caused decreased viability, oxidative stress, mitochondrial dysfunction, chromatin condensation, DNA damage, and translocation of endonuclease G to the nucleus, which was inhibited by Piracetam cotreatment, confirming that the mitochondrion-specific endonuclease G is one of the factors involved in Piracetam-induced protective mechanisms.
Dinesh Kumar Verma - One of the best experts on this subject based on the ideXlab platform.
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new therapeutic activity of metabolic enhancer Piracetam in treatment of neurodegenerative disease participation of caspase independent death factors oxidative stress inflammatory responses and apoptosis
Biochimica et Biophysica Acta, 2018Co-Authors: Dinesh Kumar Verma, Sonam Gupta, Joyshree Biswas, Neeraj Joshi, Sivarama K Raju, Abhishek Singh, Parul Gupta, Shubhangini Tiwari, Swati ChaturvediAbstract:Piracetam, a nootropic drug that has been clinically used for decades but remains enigmatic due to no distinct understanding of its mechanism of action. The present study aimed to investigate the role of caspase independent pathway in Piracetam mediated neuroprotection. LPS administration caused significant alterations in oxidative stress related parameters like glutathione, glutathione reductase and increased lipid peroxidation. LPS administration also caused augmented expression of inflammatory cytokines and astrocytes activation. Piracetam treatment offered significant protection against LPS induced oxidative and inflammatory parameters and inhibited astrocytes activation. LPS administration caused augmented level of reactive oxygen species and depleted mitochondrial membrane potential which were attenuated with Piracetam treatment. This study for the first time demonstrates the role of caspase independent death factors in Piracetam induced neuroprotective effects in rat brain. Translocation of mitochondrial resident apoptosis inducing factor and endonuclease G to nucleus through cytosol after LPS administration was significantly blocked with Piracetam treatment. Further, LPS induced DNA fragmentation along with up regulated Poly [ADP-ribose] polymerase 1 (PARP1) levels were also inhibited with Piracetam treatment. Apoptotic death was confirmed by the cleavage of caspase 3 as well as histological alteration in rat brain regions. LPS administration caused significantly increased level of cleaved caspase 3, altered neuronal morphology and decreased neuronal density which were restored with Piracetam treatment. Collectively our findings indicate that Piracetam offered protection against LPS induced inflammatory responses and cellular death including its antioxidative antiapoptotic activity with its attenuation against mitochondria mediated caspase independent pathway.
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metabolic enhancer Piracetam attenuates the translocation of mitochondrion specific proteins of caspase independent pathway poly adp ribose polymerase 1 up regulation and oxidative dna fragmentation
Neurotoxicity Research, 2018Co-Authors: Dinesh Kumar Verma, Sonam Gupta, Joyshree Biswas, Neeraj Joshi, Sivarama K Raju, Mu Wahajuddin, Sarika SinghAbstract:Piracetam, a nootropic drug, has been clinically used for decades; however, its mechanism of action still remains enigmatic. The present study was undertaken to evaluate the role of mitochondrion-specific factors of caspase-independent pathway like apoptotic-inducing factor (AIF) and endonuclease-G (endo-G) in Piracetam-induced neuroprotection. N2A cells treated with lipopolysaccharide (LPS) exhibited significant cytotoxicity, impaired mitochondrial activity, and reactive oxygen species generation which was significantly attenuated with Piracetam co-treatment. Cells co-treated with LPS and Piracetam exhibited significant uptake of Piracetam in comparison to only Piracetam-treated cells as estimated by liquid chromatography-mass spectrometry (LC-MSMS). LPS treatment caused significant translocation of AIF and endonuclease-G in neuronal N2A cells which were significantly attenuated with Piracetam co-treatment. Significant over-expression of proinflammatory cytokines was also observed after treatment of LPS to cells which was inhibited with Piracetam co-treatment demonstrating its anti-inflammatory property. LPS-treated cells exhibited significant oxidative DNA fragmentation and poly [ADP-ribose] polymerase-1 (PARP-1) up-regulation in nucleus, both of which were attenuated with Piracetam treatment. Antioxidant melatonin but not z-VAD offered the inhibited LPS-induced DNA fragmentation indicating the involvement of oxidative DNA fragmentation. Further, we did not observe the altered caspase-3 level after LPS treatment initially while at a later time point, significantly augmented level of caspase-3 was observed which was not inhibited with Piracetam treatment. In total, our findings indicate the interference of Piracetam in mitochondrion-mediated caspase-independent pathway, as well as its anti-inflammatory and antioxidative properties. Graphical Abstract Graphical abstract indicating the novel interference of metabolic enhancer Piracetam (P) in neuronal death mechanisms.
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metabolic enhancer Piracetam attenuates rotenone induced oxidative stress a study in different rat brain regions
Acta Neurobiologiae Experimentalis, 2015Co-Authors: Dinesh Kumar Verma, Neeraj Joshi, Kunumuri Sivarama Raju, Muhammad Wahajuddin, R K Singh, Sarika SinghAbstract:Piracetam is clinically being used nootropic drug but the details of its neuroprotective mechanism are not well studied. The present study was conducted to assess the effects of Piracetam on rotenone induced oxidative stress by using both ex vivo and in vivo test systems. Rats were treated with Piracetam (600 mg/kg b.w. oral) for seven constitutive days prior to rotenone administration (intracerebroventricular, 12 µg) in rat brain. Rotenone induced oxidative stress was assessed after 1 h and 24 h of rotenone administration. Ex vivo estimations were performed by using two experimental designs. In one experimental design the rat brain homogenate was treated with rotenone (1 mM, 2 mM and 4 mM) and rotenone+Piracetam (10 mM) for 1 h. While in second experimental design the rats were pretreated with Piracetam for seven consecutive days. On eighth day the rats were sacrificed, brain homogenate was prepared and treated with rotenone (1 mM, 2 mM and 4mM) for 1h. After treatment the glutathione (GSH) and malondialdehyde (MDA) levels were estimated in brain homogenate. In vivo study showed that pretreatment of Piracetam offered significant protection against rotenone induced decreased GSH and increased MDA level though the protection was region specific. But the co-treatment of Piracetam with rotenone did not offer significant protection against rotenone induced oxidative stress in ex vivo study. Whereas ex vivo experiments in rat brain homogenate of Piracetam pretreated rats, showed the significant protection against rotenone induced oxidative stress. Findings indicated that pretreatment of Piracetam significantly attenuated the rotenone induced oxidative stress though the protection was region specific. Piracetam treatment to rats led to its absorption and accumulation in different brain regions as assessed by liquid chromatography mass spectrometry/mass spectrometry. In conclusion, study indicates the Piracetam is able to enhance the antioxidant capacity in brain cells in region specific manner. The study is also revealing the rationale for its clinical use in cognitive impairment and other neurological diseases.
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The metabolic enhancer Piracetam attenuates mitochondrion-specific endonuclease G translocation and oxidative DNA fragmentation.
Free radical biology & medicine, 2014Co-Authors: Sonam Gupta, Dinesh Kumar Verma, Joyshree Biswas, K. Siva Rama Raju, Neeraj Joshi, Wahajuddin, Sarika SinghAbstract:This study was performed to investigate the involvement of mitochondrion-specific endonuclease G in Piracetam (P)-induced protective mechanisms. Studies have shown the antiapoptotic effects of Piracetam but the mechanism of action of Piracetam is still an enigma. To assess the involvement of endonuclease G in Piracetam-induced protective effects, astrocyte glial cells were treated with lipopolysaccharide (LPS) and Piracetam. LPS treatment caused significantly decreased viability, mitochondrial activity, oxidative stress, chromatin condensation, and DNA fragmentation, which were attenuated by Piracetam cotreatment. Cotreatment of astrocytes with Piracetam showed its significantly time-dependent absorption as observed with high-performance liquid chromatography. Astrocytes treated with Piracetam alone showed enhanced mitochondrial membrane potential (MMP) in comparison to control astrocytes. However, in LPS-treated cells no significant alteration in MMP was observed in comparison to control cells. Protein and mRNA levels of the terminal executor of the caspase-mediated pathway, caspase-3, were not altered significantly in LPS or LPS + Piracetam-treated astrocytes, whereas endonuclease G was significantly translocated to the nucleus in LPS-treated astrocytes. Piracetam cotreatment attenuated the LPS-induced endonuclease G translocation. In conclusion this study indicates that LPS treatment of astrocytes caused decreased viability, oxidative stress, mitochondrial dysfunction, chromatin condensation, DNA damage, and translocation of endonuclease G to the nucleus, which was inhibited by Piracetam cotreatment, confirming that the mitochondrion-specific endonuclease G is one of the factors involved in Piracetam-induced protective mechanisms.