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środa, 7 września 2016

Lyrica, Neurontin leki niszczace mozg

Byron J. Richards

Neurontin i jego nowsza wersja silniejsza, Lyrica.

Te leki zostały zatwierdzone do użytku przez FDA mimo że nie mieli pojęcia, co faktycznie dzieje się  w mózgu po ich zazywaniu.

Wstrząsające nowe badanie pokazuje, że  leki te blokują powstawanie  nowych połączeń synaptycznych.

Leki te powodują zanikanie mózgu szybciej niż jakiejkolwiek inne substancjie znane ludzkości.

Neurontin został zatwierdzony przez FDA jako lek przy  leczeniu padaczki  w 1994 roku lek przeszedł ogromną nielegalną promocję off-label, która  kosztowała Warner-Lambert 430 milionów dolarów (to pierwsza duża grzywna za promocję off-label). Lek jest obecnie własnością firmy Pfizer. Pfizer jest również właścicielem Lyrica, super-silna wersja Neurontin. Został zatwierdzony przez FDA do  leczenia różnych rodzajów bólu i fibromialgii. Lyrica jest jednym z czterech leków, które spółka  Pfizer wprowadzila nielegalnie do obrotu, w wyniku czego musi zaplacic ugode w wysokości 2,3 mld USD. Mimo, że obrót tymi lekami został surowo zakazany,nadal lekarze używają ich do leczenia wszelkiego rodzaju problemów nerwowych ponieważ są one dobre do tłumienia objawów.

Naukowcy w powyższym badaniu próbują bagatelizować poważny charakter leków mówiąc ze "neurony u dorosłych  nie tworzą wiele nowych synaps." To jest po prostu nieprawda. Nowa nauka pokazuje, że zdrowie mózgu podczas starzenia polega również na tworzeniu nowych synaps.

http://ushealthcure.com/clinical-research-finds-neurontin-and-lyrica-are-a-death-sentence-for-new-brain-synapses/

Study Abstract:

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. 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. We show that the VWF-A domain of α2δ-1 interacts with the epidermal growth factor-like repeats common to all thrombospondins. α2δ-1 overexpression increases synaptogenesis in vitro and in vivo and is required postsynaptically for thrombospondin- and astrocyte-induced synapse formation in vitro. 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.
From press release:
Researchers at the Stanford University School of Medicine have identified a key molecular player in guiding the formation of synapses — the all-important connections between nerve cells — in the brain. This discovery, based on experiments in cell culture and in mice, could advance scientists’ understanding of how young children’s brains develop as well as point to new approaches toward countering brain disorders in adults.
The new work also pinpoints, for the first time, the biochemical mechanism by which the widely prescribed drug gabapentin (also marketed under the trade name Neurontin) works. “We have solved the longstanding mystery of how this blockbuster drug acts,” said Ben Barres, MD, PhD, professor and chair of neurobiology. The study shows that gabapentin halts the formation of new synapses, possibly explaining its therapeutic value in mitigating epileptic seizures and chronic pain. This insight, however, may lead physicians to reconsider the circumstances in which the drug should be prescribed to pregnant women.
The paper, to be published online Oct. 8 in the journal Cell, looks at the interaction between neurons — the extensively researched nerve cells that account for 10 percent of the cells in the brain — and the less-studied but much more common brain cells called astrocytes. Much work has been done on how neurons transmit electrical signals to each other through synapses — the nanoscale electrochemical contact points between neurons. It is the brain’s circuitry of some 100 trillion of these synapses that allow us to think, feel, remember and move.
It is commonly agreed that the precise placement and strength of each person’s trillions of synaptic connections closely maps with that person’s cognitive, emotional and behavioral makeup. But exactly why a particular synapse is formed in a certain place at a certain time has largely remained a mystery. In 2005, Barres took a big step toward explaining this process when he and his colleagues discovered that a protein astrocytes secrete, called thrombospondin, is essential to the formation of this complex brain circuitry....

http://www.wellnessresources.com/studies/neurontin_and_lyrica_are_highly_toxic_to_new_brain_synapses/

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Neurontin and Lyrica – two treatments for pain that can lead to suicidal thoughts

Neurontin (gabapentin) and the newer Lyrica (pregabalin) are two anticonvulsant and analgesic medications originally prescribed for the treatment of epilepsy. Neurontin was originally licensed in the United States and Canada in December 1993 for use as an adjuvant medication to treat seizures and epilepsy. Lyrica on the other hand, is a much newer drug that received approval for use in the treatment of epilepsy, diabetic neuropathic pain, and pos-therpetic neuralgia in 2005, and is considered as a much more powerful version of gabapentin itself. In June 2007, Lyrica was also approved as a treatment for fibromyalgia. The mechanism of action of these two drugs is still partially unknown to medical science, but they’re though to be able to reduce the production of some neurotransmitters in the brain that are deemed responsible for pain and convulsions.
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Dangers and side effects of Neurontin (Gabapentin) and Lyrica (Pregabalin)

The main issue about the off-label marketing of these two drugs, is that neither of one is devoid of serious side effects. The dangers associated with the use of Neurontin and Lyrica are quite significant instead, and may even pose patient’s lives at risk. According to the US Food and Drug Administration (FDA), these antiepileptic drugs (AEDs) do in fact “increase the risk of suicidal thoughts or behavior in patients taking these drugs for any indication. Patients treated with any AED for any indication should be monitored for the emergence or worsening of depression, suicidal thoughts or behavior, and/or any unusual changes in mood or behavior [8]”. Subsequent researches confirmed a strict association between suicidal behaviors and use of gabapentin and pregabalin, which can be even more dangerous as an overdose of this drug can prove to be fatal, especially if combined with alcohol in case of intentional ingestion [9].

http://medsnews.com/health/neurontin-and-lyrica-two-treatments-for-pain-that-can-lead-to-suicidal-thoughts/
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The Gabapentin Receptor α2δ-1 is the Neuronal Thrombospondin Receptor Responsible for Excitatory CNS Synaptogenesis

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 CNS synaptogenesis. 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. We show that the VWF-A domain of α2δ–1 interacts with the epidermal growth factor-like repeats common to all thrombospondins. α2δ–1 overexpression increases synaptogenesis in vitro and in vivo and is required postsynaptically for thrombospondin and astrocyte-induced synapse formation in vitro. 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.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2791798/
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Neurontin and its newer more potent version, Lyrica, are widely used for off-label indications that are an outright flagrant danger to the public. These blockbuster drugs were approved for use even though the FDA had no idea what they actually did in the brain. A shocking new study shows that they block the formation of new brain synapses1, drastically reducing the potential for rejuvenating brain plasticity – meaning that these drugs will cause brain decline faster than any substance known to mankind.

http://www.wellnessresources.com/freedom/articles/neurontin_and_lyrica_are_a_death_sentence_for_new_brain_synapses/#ref1
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Study pinpoints key mechanism in brain development, raising questions about use of antiseizure drug

“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, doctors have the view that gabapentin is the safest anticonvulsant. There is no question that pregnant women with epilepsy who have been advised by their neurologists to continue their anticonvulsant treatment with gabapentin during their pregnancy should definitely remain on this drug until instructed otherwise. 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.”

https://med.stanford.edu/news/all-news/2009/10/study-pinpoints-key-mechanism-in-brain-development-raising-questions-about-use-of-antiseizure-drug.html
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https://www.drugs.com/answers/lyrica-gabapentin-thoughts-1080372.html

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