Kan du ge en kort sammanfattning? Många postar text som de kopierat och som de själva inte läst, eller läst och inte förstått.
Citat:
Här är en bättre länk,
Neurontin and Lyrica are Highly Toxic to New Brain Synapses
http://www.wellnessresources.com/studies/neurontin_and_lyrica_are_highly_toxic_to_new_brain _synapses/
Synapses are asymmetric cellular adhesions that are critical for nervous system development and function, but the mechanisms that induce their formation are not well understood. We have previously identified thrombospondin as an astrocyte-secreted protein that promotes central nervous system (CNS) synaptogenesis."
thrombospondin gynnar skapandet av nya synapser i CNS
"Here, we identify the neuronal thrombospondin receptor involved in CNS synapse formation as α2δ-1, the receptor for the anti-epileptic and analgesic drug gabapentin."
Receptorn som thrombospondin verkar på är α2δ-1
Gabapentin/Lyrica/Pregabalin verkar på α2δ-1 receptorn (samma receptor)
"Gabapentin antagonizes thrombospondin binding to α2δ-1 and powerfully inhibits excitatory synapse formation in vitro and in vivo. These findings identify α2δ-1 as a receptor involved in excitatory synapse formation and suggest that gabapentin may function therapeutically by blocking new synapse formation."
Antagonize=stänger av, simpelt förklarat förståss.
Gabapentin/Lyrica/Pregabalin stänger av så att thrombospondin inte kan verka på receptorn (α2δ-1) som gynnar skapandet av synapser i CNS
"In their new study, Barres and his colleagues found that when gabapentin was administered in developing mice, it bound to alpha2delta-1(α2δ-1), preventing thrombospondin from binding to the receptor and, in turn, impeding synapse formation. Likewise, by blocking thrombosponin, gabapentin may reduce excess synapse formation in vulnerable areas of the human brain."
Gabapentin/Lyrica/Pregabalin stänger av så att thrombospondin inte kan verka på receptorn (α2δ-1) som gynnar skapandet av synapser i CNS
"Barres noted that he and his colleagues found that gabapentin does not dissolve pre-existing synapses, but only prevents formation of new ones. That greatly diminishes gabapentin’s potential danger to adults."
"But the new findings raise questions about gabapentin’s effect in situations where synapse formation is widespread and crucial, most notably in pregnancies. The vast bulk of the brain’s synapses are formed during gestation and the very early months and years after birth. Because gabapentin easily crosses the placental barrier, it could potentially interfere with a fetus’ rapidly developing brain just when global synapse formation is proceeding at breakneck speed."
“It’s a bit scary that a drug that can so powerfully block synapse formation is being used in pregnant women,” Barres said. “This potential effect on fetal brains needs to be taken seriously. Right now, 2009 October, doctors have the view that gabapentin is the safest anticonvulsant."
"But there is no long-term registry being kept to track gabapentin-exposed babies. Our findings are saying that we need to be following up on these newborns so that their cognitive performance can be studied as they grow older.”
Här är något iaf.
Study Information:
Çagla Eroglu, Nicola J. Allen, Michael W. Susman, Nancy A. O'Rourke, Chan Young Park, Engin Özkan, Chandrani Chakraborty, Sara B. Mulinyawe, Douglas S. Annis, Andrew D. Huberman, Eric M. Green, Jack Lawler, Ricardo Dolmetsch, K. Christopher Garcia, Stephen Gabapentin Receptor α2δ-1 Is a Neuronal Thrombospondin Receptor Responsible for Excitatory CNS Synaptogenesis Cell 2009 October
Stanford University School of Medicine.
Intressant tråd,
http://www.bluelight.org/vb/threads/659256-lyrica-s-(pregabalin-s)-real-mechanisim
"I'm glad you're interested in the pharmacology... more than a lot of people around here. But you are WAAAAY oversimplifying the mechanisms of NMDA and what an antagonist or agonist could cause down stream. Some antagonists have completely different effects when bound to the same exact site on NMDAR's that other antagonists bind to. It isn't that simple. NDMA and glutamate in general are such basic and broad transmitters that they aren't easily predictable, ever. And to theorize that pregablin can fix all these problems because an nmda antagonist should downstream activate x and y which have been implicated in some cardiac problems doesn't mean it will. hell x and y could be implicated in cardiac problems as a side effect downstream from something else's feedback loop. Unfortunately we're just beginning to scratch the surface of glutamatergic potential. It has the ability to cause sedation/dissociation/hallucination/anxiolysis/amnesia/anesthesia/and even psychosis that mimics 100% schizophrenia all from JUST antagonists. It's such a main component of our system and it's wired and connected to so much of our CNS that we just can't make speculations like that because while they could be right, they are more than likely wrong.
Gabapentin Pregabalin Atagabalin and all the other gabalins seem to cause carcinoma's. They did in vitro and they did in mice in vivo. Why? I have no idea. The current theory is they may actually work by also stopping new cells and nerves from growing/forming connections and they don't even know if that's true how it causes that. Could it interfere with apoptosis, maybe? Could something messing with our cells basic control loops cause cancer, absolutely. But it's only speculation at this point. What isn't speculation is that it does seem to cause cancer. There are many studies on it. Infact, gabapentin extended release was tried to be brought on patent and the FDA denied it specifically because of it's carcinogenic potential. It wasn't a special molecule it was just an extended release version of gabapentin. But gabapentin was approved. Why? Because sometimes the drug companies get their way, but I like to think the FDA wised up. Had gabapentin been brought out now it would be denied. It was approved as an adjunct and last line of treatment for seizures that don't respond to anything else, and the data showed it really didn't help seizures anyways. But it was touted as a wonder drug, research started appearing saying it was good at curing pain nerve pain fibromyalgia, anxiety, insomnia everything it was a miracle. And that's why Pfizer got hit with that enormous 430 million dollar (and now another 141 million) settlement/lawsuit. The research on gabapentin was falsified by pfizer. They realized they were going to make no money on the drug when the fda approved it as an adjunect to other seizure meds, and they had marketing teams type up research papers and publish them as fact, the pushed it off label for everything and doctored their market-made research publications to reflect that gabapentin worked wonders for every single problem. They got in a LOT of trouble. 90% of the research on gabapentin is under scrutiny and what has been looked at by investigators (the FDA research given to the FDA by Pfizer with data on their drug) which was used to get the drug approved, turned out to be so scientifically flawed that there was no way it had ever actually been done. It literally was made up in a board room and then some doctor was paid to put his name on it.
Anyway look up the cancer thing no joke there."
Neurontin and Lyrica are Highly Toxic to New Brain Synapses
http://www.wellnessresources.com/studies/neurontin_and_lyrica_are_highly_toxic_to_new_brain _synapses/
Synapses are asymmetric cellular adhesions that are critical for nervous system development and function, but the mechanisms that induce their formation are not well understood. We have previously identified thrombospondin as an astrocyte-secreted protein that promotes central nervous system (CNS) synaptogenesis."
thrombospondin gynnar skapandet av nya synapser i CNS
"Here, we identify the neuronal thrombospondin receptor involved in CNS synapse formation as α2δ-1, the receptor for the anti-epileptic and analgesic drug gabapentin."
Receptorn som thrombospondin verkar på är α2δ-1
Gabapentin/Lyrica/Pregabalin verkar på α2δ-1 receptorn (samma receptor)
"Gabapentin antagonizes thrombospondin binding to α2δ-1 and powerfully inhibits excitatory synapse formation in vitro and in vivo. These findings identify α2δ-1 as a receptor involved in excitatory synapse formation and suggest that gabapentin may function therapeutically by blocking new synapse formation."
Antagonize=stänger av, simpelt förklarat förståss.
Gabapentin/Lyrica/Pregabalin stänger av så att thrombospondin inte kan verka på receptorn (α2δ-1) som gynnar skapandet av synapser i CNS
"In their new study, Barres and his colleagues found that when gabapentin was administered in developing mice, it bound to alpha2delta-1(α2δ-1), preventing thrombospondin from binding to the receptor and, in turn, impeding synapse formation. Likewise, by blocking thrombosponin, gabapentin may reduce excess synapse formation in vulnerable areas of the human brain."
Gabapentin/Lyrica/Pregabalin stänger av så att thrombospondin inte kan verka på receptorn (α2δ-1) som gynnar skapandet av synapser i CNS
"Barres noted that he and his colleagues found that gabapentin does not dissolve pre-existing synapses, but only prevents formation of new ones. That greatly diminishes gabapentin’s potential danger to adults."
"But the new findings raise questions about gabapentin’s effect in situations where synapse formation is widespread and crucial, most notably in pregnancies. The vast bulk of the brain’s synapses are formed during gestation and the very early months and years after birth. Because gabapentin easily crosses the placental barrier, it could potentially interfere with a fetus’ rapidly developing brain just when global synapse formation is proceeding at breakneck speed."
“It’s a bit scary that a drug that can so powerfully block synapse formation is being used in pregnant women,” Barres said. “This potential effect on fetal brains needs to be taken seriously. Right now, 2009 October, doctors have the view that gabapentin is the safest anticonvulsant."
"But there is no long-term registry being kept to track gabapentin-exposed babies. Our findings are saying that we need to be following up on these newborns so that their cognitive performance can be studied as they grow older.”
Här är något iaf.
Study Information:
Çagla Eroglu, Nicola J. Allen, Michael W. Susman, Nancy A. O'Rourke, Chan Young Park, Engin Özkan, Chandrani Chakraborty, Sara B. Mulinyawe, Douglas S. Annis, Andrew D. Huberman, Eric M. Green, Jack Lawler, Ricardo Dolmetsch, K. Christopher Garcia, Stephen Gabapentin Receptor α2δ-1 Is a Neuronal Thrombospondin Receptor Responsible for Excitatory CNS Synaptogenesis Cell 2009 October
Stanford University School of Medicine.
Intressant tråd,
http://www.bluelight.org/vb/threads/659256-lyrica-s-(pregabalin-s)-real-mechanisim
"I'm glad you're interested in the pharmacology... more than a lot of people around here. But you are WAAAAY oversimplifying the mechanisms of NMDA and what an antagonist or agonist could cause down stream. Some antagonists have completely different effects when bound to the same exact site on NMDAR's that other antagonists bind to. It isn't that simple. NDMA and glutamate in general are such basic and broad transmitters that they aren't easily predictable, ever. And to theorize that pregablin can fix all these problems because an nmda antagonist should downstream activate x and y which have been implicated in some cardiac problems doesn't mean it will. hell x and y could be implicated in cardiac problems as a side effect downstream from something else's feedback loop. Unfortunately we're just beginning to scratch the surface of glutamatergic potential. It has the ability to cause sedation/dissociation/hallucination/anxiolysis/amnesia/anesthesia/and even psychosis that mimics 100% schizophrenia all from JUST antagonists. It's such a main component of our system and it's wired and connected to so much of our CNS that we just can't make speculations like that because while they could be right, they are more than likely wrong.
Gabapentin Pregabalin Atagabalin and all the other gabalins seem to cause carcinoma's. They did in vitro and they did in mice in vivo. Why? I have no idea. The current theory is they may actually work by also stopping new cells and nerves from growing/forming connections and they don't even know if that's true how it causes that. Could it interfere with apoptosis, maybe? Could something messing with our cells basic control loops cause cancer, absolutely. But it's only speculation at this point. What isn't speculation is that it does seem to cause cancer. There are many studies on it. Infact, gabapentin extended release was tried to be brought on patent and the FDA denied it specifically because of it's carcinogenic potential. It wasn't a special molecule it was just an extended release version of gabapentin. But gabapentin was approved. Why? Because sometimes the drug companies get their way, but I like to think the FDA wised up. Had gabapentin been brought out now it would be denied. It was approved as an adjunct and last line of treatment for seizures that don't respond to anything else, and the data showed it really didn't help seizures anyways. But it was touted as a wonder drug, research started appearing saying it was good at curing pain nerve pain fibromyalgia, anxiety, insomnia everything it was a miracle. And that's why Pfizer got hit with that enormous 430 million dollar (and now another 141 million) settlement/lawsuit. The research on gabapentin was falsified by pfizer. They realized they were going to make no money on the drug when the fda approved it as an adjunect to other seizure meds, and they had marketing teams type up research papers and publish them as fact, the pushed it off label for everything and doctored their market-made research publications to reflect that gabapentin worked wonders for every single problem. They got in a LOT of trouble. 90% of the research on gabapentin is under scrutiny and what has been looked at by investigators (the FDA research given to the FDA by Pfizer with data on their drug) which was used to get the drug approved, turned out to be so scientifically flawed that there was no way it had ever actually been done. It literally was made up in a board room and then some doctor was paid to put his name on it.
Anyway look up the cancer thing no joke there."
