liftsiron
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posted by marilia05 on CEM
piracetam
Bellow you will find a couple of more or less recent bib references on piracetam's effect on restoring brain function in aging, accidents, diseases and other occurrences.
HOWEVER (!!) it has been lately considered some sort of "magic bullet" for focus and cognitive improvement in general, which obviously has it's application in sports. Especially in strength sports that require EXTREME concentration for the perfect execution of one maximum effort movement, such as both liftings.
What do you think?
Piracetam--an old drug with novel properties?
Winnicka K, Tomasiak M, Bielawska A.
Department of Drug Technology, Medical University of Bialystok, 1 Kilinskiego Str., 15-089 Bialystok, Poland.
Piracetam (2-oxo-1-pyrrolidine-acetamide), the most common of the nootropic drugs, is a cyclic derivative of gamma-aminobutyric acid. The treatment with piracetam improves learning, memory, brain metabolism, and capacity. Piracetam has been shown to alter the physical properties of the plasma membrane by increasing its fluidity and by protecting the cell against hypoxia. It increases red cell deformability and normalizes aggregation of hyperactive platelets. Piracetam is an agent with antithrombotic, neuroprotective and rheological properties. The interaction of this molecule with the membrane phospholipids restores membrane fluidity and could explain the efficacy of piracetam in various disorders ranging from dementia and vertigo to myoclonus and stroke.
Publication Types:
Review
PMID: 16459490 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
2: Pharmacopsychiatry. 1999 Mar;32 Suppl 1:2-9. Related Articles, Links
Piracetam: novelty in a unique mode of action.
Muller WE, Eckert GP, Eckert A.
Department of Pharmacology, Biocenter University of Frankfurt, Germany.
Extensive research of the recent years has demonstrated that piracetam is effective in the treatment of cognitive decline in aging and dementia. It is usually much more active in situations of impaired brain function. Accordingly, its mechanism of action has been associated with neurochemical deficits of the aged brain relevant to cognitive dysfunctions. Since many of these neurochemical deficits depend on changes of membrane properties, including fluidity, it is of special importance that piracetam not only modifies membrane properties by interacting with the polar head moieties of the phospholipid bilayer, but also that this effect is more pronounced in membranes of aged as opposed to young animal and human brains, and that this mechanism also has specific relevance for brain membranes of Alzheimer's disease patients. Altering membrane properties might also be involved in vascular effects of piracetam such as improved erythrocyte deformability and normalization of hyperactive platelet aggregation. This novel mechanism of piracetam thus combines a rather non-specific physico-chemical mode of action with the pharmacological and clinical experience with this unique drug - effects are always much more pronounced when function is impaired.
Publication Types:
Review
PMID: 10338102 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
3: CNS Drug Rev. 2005 Summer;11(2):169-82. Related Articles, Links
Piracetam: a review of pharmacological properties and clinical uses.
Winblad B.
Karolinska Institutet, Neurotec, Huddinge, University Hospital B 84, S-14186 Stockholm, Sweden. [email protected]
Piracetam, a derivative of the neurotransmitter gamma-aminobutyric acid (GABA), has a variety of physiological effects that may result, at least in part, from the restoration of cell membrane fluidity. At a neuronal level, piracetam modulates neurotransmission in a range of transmitter systems (including cholinergic and glutamatergic), has neuroprotective and anticonvulsant properties, and improves neuroplasticity. At a vascular level, it appears to reduce erythrocyte adhesion to vascular endothelium, hinder vasospasm, and facilitate microcirculation. This diverse range of physiological effects is consistent with its use in a range of clinical indications. Its efficacy is documented in cognitive disorders and dementia, vertigo, cortical myoclonus, dyslexia, and sickle cell anemia. While high doses are sometimes necessary, piracetam is well tolerated.
Publication Types:
Review
PMID: 16007238 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
4: Epileptic Disord. 2000 Jun;2(2):99-105. Related Articles, Links
Piracetam and levetiracetam: close structural similarities but different pharmacological and clinical profiles.
Genton P, Van Vleymen B.
Centre Saint-Paul, Marseille, France. [email protected]
Piracetam (PIR) and levetiracetam (LEV), an S-enantiomer, are pyrrolidone derivatives that share similar chemical structures but have distinct pharmacological profiles and consequently different clinical uses. Although the mode of action of neither drug has been fully elucidated, they do not interact with inhibitory or excitatory neurotransmission or alter membrane excitability. A brain-specific stereoselective binding site has been identified for which LEV and other S-enantiomers, but not PIR, have high affinity. In preclinical studies, PIR significantly improves learning and memory; in contrast, LEV has less effect but is much more active in preventing seizures. Both drugs have a high therapeutic index and are well tolerated. PIR, a nootropic drug, is used in the therapy of age-related cognitive disturbances and poststroke aphasia. Clinical experience has also shown that at high doses it is effective against cortical myoclonus. LEV is an antiepileptic drug. Clinical trials have confirmed its efficacy in partial seizures and preliminary findings suggest that it is also effective in generalized seizures and myoclonus.
Publication Types:
Review
PMID: 10954241 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
5: Pharmacopsychiatry. 1999 Mar;32 Suppl 1:44-8. Related Articles, Links
Piracetam and platelets--a review of laboratory and clinical data.
Evers S, Grotemeyer KH.
Department of Neurology, University of Munster, Germany.
This paper reviews the effects of piracetam on platelet function and the evidence for its antiplatelet effect which is mediated mainly by inhibition of platelet aggregation. Piracetam also possesses antithrombotic activity in vivo. It has been shown to normalize platelet aggregation in patients with increased platelet aggregability in various disorders including acute stroke, transient cerebral ischemic attacks and diabetes mellitus. This, together with clinical improvement, has also been shown in patients with Raynaud's phenomenon. The results of recent studies are presented in which piracetam showed similar efficacy to aspirin in the secondary prophylaxis of ischemic stroke.
Publication Types:
Review
PMID: 10338108 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
6: Crit Rev Neurobiol. 1996;10(3-4):357-70. Related Articles, Links
Nootropics: preclinical results in the light of clinical effects; comparison with tacrine.
Mondadori C.
Hoechst Marion Roussel, CNS Research, Bridgewater, NJ 08807-0800, USA.
This review is meant to serve several purposes. First, it surveys the preclinical and clinical profiles of piracetam-like nootropics. Second, the conditions under which the nootropics are active in preclinical studies are identified and analyzed with a view of finding a common denominator that could explain the observed effects. Third, the clinical profile is examined, on the one hand to assess whether these drugs are in fact active in humans, and on the other to determine how the clinical effects of the nootropics compare with those of tacrine. Lastly, the clinical data are then further scrutinized to assess whether they fulfill the expectations based on the preclinical findings.
Publication Types:
Comparative Study
Review
PMID: 8978986 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
7: Br J Pharmacol. 2004 Jun;142(3):594-608. Epub 2004 May 17. Related Articles, Links
Piracetam and TRH analogues antagonise inhibition by barbiturates, diazepam, melatonin and galanin of human erythrocyte D-glucose transport.
Naftalin RJ, Cunningham P, Afzal-Ahmed I.
Physiology Division, Centre for Vascular Biology and Medicine, King's College London, Guy's Campus, New Hunt's House, London SE1 1UL. [email protected]
1 Nootropic drugs increase glucose uptake into anaesthetised brain and into Alzheimer's diseased brain. Thyrotropin-releasing hormone, TRH, which has a chemical structure similar to nootropics increases cerebellar uptake of glucose in murine rolling ataxia. This paper shows that nootropic drugs like piracetam (2-oxo 1 pyrrolidine acetamide) and levetiracetam and neuropeptides like TRH antagonise the inhibition of glucose transport by barbiturates, diazepam, melatonin and endogenous neuropeptide galanin in human erythrocytes in vitro. 2 The potencies of nootropic drugs in opposing scopolamine-induced memory loss correlate with their potencies in antagonising pentobarbital inhibition of erythrocyte glucose transport in vitro (P<0.01). Less potent nootropics, D-levetiracetam and D-pyroglutamate, have higher antagonist Ki's against pentobarbital inhibition of glucose transport than more potent L-stereoisomers (P<0.001). 3 Piracetam and TRH have no direct effects on net glucose transport, but competitively antagonise hypnotic drug inhibition of glucose transport. Other nootropics, like aniracetam and levetiracetam, while antagonising pentobarbital action, also inhibit glucose transport. Analeptics like bemigride and methamphetamine are more potent inhibitors of glucose transport than antagonists of hypnotic action on glucose transport. 4 There are similarities between amino-acid sequences in human glucose transport protein isoform 1 (GLUT1) and the benzodiazepine-binding domains of GABAA (gamma amino butyric acid) receptor subunits. Mapped on a 3D template of GLUT1, these homologies suggest that the site of diazepam and piracetam interaction is a pocket outside the central hydrophilic pore region. 5 Nootropic pyrrolidone antagonism of hypnotic drug inhibition of glucose transport in vitro may be an analogue of TRH antagonism of galanin-induced narcosis.
PMID: 15148255 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
8: Pharmacopsychiatry. 1999 Mar;32 Suppl 1:10-6. Related Articles, Links
Piracetam improves cognitive performance by restoring neurochemical deficits of the aged rat brain.
Scheuer K, Rostock A, Bartsch R, Muller WE.
Department of Psychopharmacology, Central Institute of Mental Health Mannheim, Germany.
In order to test the hypothesis that piracetam improves cognitive functions by restoring biochemical deficits of the aging brain, we investigated the effects of piracetam treatment (300 mg/kg daily for 6 weeks) on the active avoidance performance of young and aged rats. After testing, the rats were killed and membrane fluidity and NMDA as well muscarinic cholinergic receptor densities were determined in the frontal cortex, the hippocampus, the striatum, as well as the cerebellum. Piracetam treatment improved active avoidance learning in the aged rats only and elevated membrane fluidity in all brain regions except the cerebellum in the aged animals. Moreover, we observed a positive effect of piracetam treatment on NMDA receptor density in the hippocampus and on muscarinic cholinergic receptor densities in the frontal cortex and the striatum and to a lesser extent in the hippocampus. Again, these effects were only observed in aged animals. Discrimination analysis indicated that piracetam effects on membrane fluidity in the frontal cortex, the hippocampus, and the striatum and its effects on NMDA densities in the hippocampus might be involved in its positive effects on cognitive performance.
Publication Types:
Research Support, Non-U.S. Gov't
PMID: 10338103 [PubMed - indexed for MEDLINE]
piracetam
Bellow you will find a couple of more or less recent bib references on piracetam's effect on restoring brain function in aging, accidents, diseases and other occurrences.
HOWEVER (!!) it has been lately considered some sort of "magic bullet" for focus and cognitive improvement in general, which obviously has it's application in sports. Especially in strength sports that require EXTREME concentration for the perfect execution of one maximum effort movement, such as both liftings.
What do you think?
Piracetam--an old drug with novel properties?
Winnicka K, Tomasiak M, Bielawska A.
Department of Drug Technology, Medical University of Bialystok, 1 Kilinskiego Str., 15-089 Bialystok, Poland.
Piracetam (2-oxo-1-pyrrolidine-acetamide), the most common of the nootropic drugs, is a cyclic derivative of gamma-aminobutyric acid. The treatment with piracetam improves learning, memory, brain metabolism, and capacity. Piracetam has been shown to alter the physical properties of the plasma membrane by increasing its fluidity and by protecting the cell against hypoxia. It increases red cell deformability and normalizes aggregation of hyperactive platelets. Piracetam is an agent with antithrombotic, neuroprotective and rheological properties. The interaction of this molecule with the membrane phospholipids restores membrane fluidity and could explain the efficacy of piracetam in various disorders ranging from dementia and vertigo to myoclonus and stroke.
Publication Types:
Review
PMID: 16459490 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
2: Pharmacopsychiatry. 1999 Mar;32 Suppl 1:2-9. Related Articles, Links
Piracetam: novelty in a unique mode of action.
Muller WE, Eckert GP, Eckert A.
Department of Pharmacology, Biocenter University of Frankfurt, Germany.
Extensive research of the recent years has demonstrated that piracetam is effective in the treatment of cognitive decline in aging and dementia. It is usually much more active in situations of impaired brain function. Accordingly, its mechanism of action has been associated with neurochemical deficits of the aged brain relevant to cognitive dysfunctions. Since many of these neurochemical deficits depend on changes of membrane properties, including fluidity, it is of special importance that piracetam not only modifies membrane properties by interacting with the polar head moieties of the phospholipid bilayer, but also that this effect is more pronounced in membranes of aged as opposed to young animal and human brains, and that this mechanism also has specific relevance for brain membranes of Alzheimer's disease patients. Altering membrane properties might also be involved in vascular effects of piracetam such as improved erythrocyte deformability and normalization of hyperactive platelet aggregation. This novel mechanism of piracetam thus combines a rather non-specific physico-chemical mode of action with the pharmacological and clinical experience with this unique drug - effects are always much more pronounced when function is impaired.
Publication Types:
Review
PMID: 10338102 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
3: CNS Drug Rev. 2005 Summer;11(2):169-82. Related Articles, Links
Piracetam: a review of pharmacological properties and clinical uses.
Winblad B.
Karolinska Institutet, Neurotec, Huddinge, University Hospital B 84, S-14186 Stockholm, Sweden. [email protected]
Piracetam, a derivative of the neurotransmitter gamma-aminobutyric acid (GABA), has a variety of physiological effects that may result, at least in part, from the restoration of cell membrane fluidity. At a neuronal level, piracetam modulates neurotransmission in a range of transmitter systems (including cholinergic and glutamatergic), has neuroprotective and anticonvulsant properties, and improves neuroplasticity. At a vascular level, it appears to reduce erythrocyte adhesion to vascular endothelium, hinder vasospasm, and facilitate microcirculation. This diverse range of physiological effects is consistent with its use in a range of clinical indications. Its efficacy is documented in cognitive disorders and dementia, vertigo, cortical myoclonus, dyslexia, and sickle cell anemia. While high doses are sometimes necessary, piracetam is well tolerated.
Publication Types:
Review
PMID: 16007238 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
4: Epileptic Disord. 2000 Jun;2(2):99-105. Related Articles, Links
Piracetam and levetiracetam: close structural similarities but different pharmacological and clinical profiles.
Genton P, Van Vleymen B.
Centre Saint-Paul, Marseille, France. [email protected]
Piracetam (PIR) and levetiracetam (LEV), an S-enantiomer, are pyrrolidone derivatives that share similar chemical structures but have distinct pharmacological profiles and consequently different clinical uses. Although the mode of action of neither drug has been fully elucidated, they do not interact with inhibitory or excitatory neurotransmission or alter membrane excitability. A brain-specific stereoselective binding site has been identified for which LEV and other S-enantiomers, but not PIR, have high affinity. In preclinical studies, PIR significantly improves learning and memory; in contrast, LEV has less effect but is much more active in preventing seizures. Both drugs have a high therapeutic index and are well tolerated. PIR, a nootropic drug, is used in the therapy of age-related cognitive disturbances and poststroke aphasia. Clinical experience has also shown that at high doses it is effective against cortical myoclonus. LEV is an antiepileptic drug. Clinical trials have confirmed its efficacy in partial seizures and preliminary findings suggest that it is also effective in generalized seizures and myoclonus.
Publication Types:
Review
PMID: 10954241 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
5: Pharmacopsychiatry. 1999 Mar;32 Suppl 1:44-8. Related Articles, Links
Piracetam and platelets--a review of laboratory and clinical data.
Evers S, Grotemeyer KH.
Department of Neurology, University of Munster, Germany.
This paper reviews the effects of piracetam on platelet function and the evidence for its antiplatelet effect which is mediated mainly by inhibition of platelet aggregation. Piracetam also possesses antithrombotic activity in vivo. It has been shown to normalize platelet aggregation in patients with increased platelet aggregability in various disorders including acute stroke, transient cerebral ischemic attacks and diabetes mellitus. This, together with clinical improvement, has also been shown in patients with Raynaud's phenomenon. The results of recent studies are presented in which piracetam showed similar efficacy to aspirin in the secondary prophylaxis of ischemic stroke.
Publication Types:
Review
PMID: 10338108 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
6: Crit Rev Neurobiol. 1996;10(3-4):357-70. Related Articles, Links
Nootropics: preclinical results in the light of clinical effects; comparison with tacrine.
Mondadori C.
Hoechst Marion Roussel, CNS Research, Bridgewater, NJ 08807-0800, USA.
This review is meant to serve several purposes. First, it surveys the preclinical and clinical profiles of piracetam-like nootropics. Second, the conditions under which the nootropics are active in preclinical studies are identified and analyzed with a view of finding a common denominator that could explain the observed effects. Third, the clinical profile is examined, on the one hand to assess whether these drugs are in fact active in humans, and on the other to determine how the clinical effects of the nootropics compare with those of tacrine. Lastly, the clinical data are then further scrutinized to assess whether they fulfill the expectations based on the preclinical findings.
Publication Types:
Comparative Study
Review
PMID: 8978986 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
7: Br J Pharmacol. 2004 Jun;142(3):594-608. Epub 2004 May 17. Related Articles, Links
Piracetam and TRH analogues antagonise inhibition by barbiturates, diazepam, melatonin and galanin of human erythrocyte D-glucose transport.
Naftalin RJ, Cunningham P, Afzal-Ahmed I.
Physiology Division, Centre for Vascular Biology and Medicine, King's College London, Guy's Campus, New Hunt's House, London SE1 1UL. [email protected]
1 Nootropic drugs increase glucose uptake into anaesthetised brain and into Alzheimer's diseased brain. Thyrotropin-releasing hormone, TRH, which has a chemical structure similar to nootropics increases cerebellar uptake of glucose in murine rolling ataxia. This paper shows that nootropic drugs like piracetam (2-oxo 1 pyrrolidine acetamide) and levetiracetam and neuropeptides like TRH antagonise the inhibition of glucose transport by barbiturates, diazepam, melatonin and endogenous neuropeptide galanin in human erythrocytes in vitro. 2 The potencies of nootropic drugs in opposing scopolamine-induced memory loss correlate with their potencies in antagonising pentobarbital inhibition of erythrocyte glucose transport in vitro (P<0.01). Less potent nootropics, D-levetiracetam and D-pyroglutamate, have higher antagonist Ki's against pentobarbital inhibition of glucose transport than more potent L-stereoisomers (P<0.001). 3 Piracetam and TRH have no direct effects on net glucose transport, but competitively antagonise hypnotic drug inhibition of glucose transport. Other nootropics, like aniracetam and levetiracetam, while antagonising pentobarbital action, also inhibit glucose transport. Analeptics like bemigride and methamphetamine are more potent inhibitors of glucose transport than antagonists of hypnotic action on glucose transport. 4 There are similarities between amino-acid sequences in human glucose transport protein isoform 1 (GLUT1) and the benzodiazepine-binding domains of GABAA (gamma amino butyric acid) receptor subunits. Mapped on a 3D template of GLUT1, these homologies suggest that the site of diazepam and piracetam interaction is a pocket outside the central hydrophilic pore region. 5 Nootropic pyrrolidone antagonism of hypnotic drug inhibition of glucose transport in vitro may be an analogue of TRH antagonism of galanin-induced narcosis.
PMID: 15148255 [PubMed - indexed for MEDLINE]
--------------------------------------------------------------------------------
8: Pharmacopsychiatry. 1999 Mar;32 Suppl 1:10-6. Related Articles, Links
Piracetam improves cognitive performance by restoring neurochemical deficits of the aged rat brain.
Scheuer K, Rostock A, Bartsch R, Muller WE.
Department of Psychopharmacology, Central Institute of Mental Health Mannheim, Germany.
In order to test the hypothesis that piracetam improves cognitive functions by restoring biochemical deficits of the aging brain, we investigated the effects of piracetam treatment (300 mg/kg daily for 6 weeks) on the active avoidance performance of young and aged rats. After testing, the rats were killed and membrane fluidity and NMDA as well muscarinic cholinergic receptor densities were determined in the frontal cortex, the hippocampus, the striatum, as well as the cerebellum. Piracetam treatment improved active avoidance learning in the aged rats only and elevated membrane fluidity in all brain regions except the cerebellum in the aged animals. Moreover, we observed a positive effect of piracetam treatment on NMDA receptor density in the hippocampus and on muscarinic cholinergic receptor densities in the frontal cortex and the striatum and to a lesser extent in the hippocampus. Again, these effects were only observed in aged animals. Discrimination analysis indicated that piracetam effects on membrane fluidity in the frontal cortex, the hippocampus, and the striatum and its effects on NMDA densities in the hippocampus might be involved in its positive effects on cognitive performance.
Publication Types:
Research Support, Non-U.S. Gov't
PMID: 10338103 [PubMed - indexed for MEDLINE]
