Neurontin and Lyrica are a death sentence for the new brain synapses

Neurontin and more powerful version,    Lyrica    , are widely used for off label indications that an immediate danger to the blatant public. The blockbuster drugs have been approved for use, although the FDA had no idea what they really the brain. A new study shows shocking that blocking the formation of new synapses brain rejuvenation possibilities of brain plasticity, a drastic reduction – that is, these drugs will lead to lower brain faster than any substance known to mankind .

The problem with these drugs is complicated by law on illegal trade. Neurontin was approved by the FDA for epilepsy in 1994. The drug has undergone huge advancement illegal off-label Warner-Lambert for $ 430 million (the first penalty for promoting off-label). The drug is now owned by Pfizer. Pfizer also has Lyrica, a super-powerful version of Neurontin. It was approved by the FDA for different types of pain and fibromyalgia. Lyrica is one of four drugs that are a subsidiary of Pfizer illegally on the market, resulting in an agreement of $ 2.3 billion against Pfizer. (details below): –

Although the sale of these drugs has fined, they continue to accumulate billions of dollars in sales of off-label use. Doctors use for all types of nerve problems, because they are good at suppressing the symptoms. However, such use can not be justified because finally understood, the actual mechanism of the drug and are creating a significant reduction in long-term health of the nerves.

The researchers said the study trying to “do not make many new synapses mature neurons. “Trivialize the seriousness of the drug by saying that is not true. The new science shows that brain health in aging is based on the formation of new synapses. Even the researchers were able to question the common use of these drugs in pregnant women. How a fetus that creates new nerve cells when the mother takes a drug that blocks?

These are the kind of situations should be all the FDA. As usual, the FDA is warning sat pondering suicide Lyrica for off-label uses include bipolar disorder and migraine. The FDA is likely to move the thumbs the next ten years on brain injury problem. Consumer Care.

Pfizer ponies up $ 2.3 billion for drug crimes

Pfizer agreed to pay $ 2.3 billion to settle civil and criminal responsibility for promoting illegal off label Bextra (already withdrawn from the market painkillers), Geodon (as Zyprexa, an atypical antipsychotic harm children) Zyvox ( an antibiotic) and Lyrica (a drug of epilepsy). Pfizer shall be guilty of an offense of violation food manager Advocate, drugs and cosmetics Bextra forgeries to defraud with intent.

The case was brought by whistleblowers sic which will be paid US $ 102 million as part of the agreement.

Geodon has a lower percentage of poisoning country $ 12 billion a year to our children and the elderly, taking about $ 750 million. It has been widely promoted as a label for the ADHD children and behavioral problems – a market that has created and continues to develop fradulaently sales.

Pfizer will find no doubt as to how these costs more as future higher costs of the drug to the US taxpayer.

Big Pharma executives for criminal has actually sent to prison for injuring and killing people to misuse drugs intentionally, this behavior does not stop risk. promoting fraudulent medicines is part of the culture of all the key players in the corrupt industry. Until this issue is resolved, there is no way to control the costs of health care.

Study Title:

Gabapentin S-1 receptor is a neuronal thrombospondin receptor responsible for the CNS stimulation Synaptogenesis

Summary of the study:

Synapses asymmetric cellular adhesions that are essential for nervous system development and function, but the mechanisms that induce the formation are not well understood. We have already identified thrombospondin secreted proteins such as astrocytes that the central nervous system (CNS) promotes synaptogenesis. Here we bring the neuronal thrombospondin receptor involved in CNS synapse as α2δ-1, the receptor for gabapentin anticonvulsant and analgesic. We show that the area α2δ VWF-A-1 cooperates with the epidermal growth factor repeats the same for all thrombospondin. α2δ-1 overexpression increases synaptogenesis in vitro and in vivo, and requires the thrombospondin- synapse formation in vitro and induced postsynaptic astrocytes. Gabapentin antagonizes the α2δ-1 binding, and strongly inhibit excitatory synapse formation in vitro and in vivo thrombospondin. These results identify α2δ-1 as a receptor involved in the formation of excitatory synapses, suggesting that the therapeutic function gabapentin May by blocking the formation of new synapses.

Press release:

Researchers at Stanford School of Medicine of the University have identified a key molecular player to guide the formation of synapses – the most important connections between nerve cells – in the brain. This discovery, to promote cell-based experiments and in mice in culture, scientists can understand how the brain development of children and to propose a new approach to the fight against brain disorders in adults.

The new work points also for the first time, the biochemical mechanism by which (also set marketed under the brand Neurontin) Gabapentin works of drugs widely prescribed. “We mystery of this blockbuster drug solved long ago,” said Ben Barres, MD, PhD, professor and chair of neurobiology. The study shows that gabapentin formation of new synapses stops may explain the therapeutic value in reducing seizures and chronic pain. However, this perception can lead doctors to circumstances in which the drug should be prescribed to pregnant women to reconsider.

The print, online October 8 are published in the journal Cell, examines the interaction between neurons – nerve cells in-depth studies, which represent 10 percent of the cells in the brain – and less studied, but many more cells brain called astrocytes. Much work has been done as the neurons transmit electrical signals to each other by synapses – an electrochemical contact nanoscale between neurons. The circuit around 100000000000000 synapses that allow us to think, feel, remember and move the brain.

It is generally accepted that the exact positioning and strength of each person trillion synaptic connections closely maps to cognitive composition, emotional and behavioral of the person. But exactly why a particular synapse is formed largely remained a mystery in a certain place at a certain time. In 2005, made a great Barres not explain the process by himself and his colleagues found that astrocytes secrete a protein called thrombospondin, is essential for the formation of these circuits complex brains.

But no one knew the exact mechanism by which the formation of synapses induced thrombospondin.

In this new study, Barres, author Cagla Eroglu, Ph.D., and his colleagues have shown that thrombospondin alloy to a receptor on the outer membrane of neurons. The role of this receptor, known as alpha2delta-1 name was obscure until now. But in an experiment with mice, the scientists found that neurons that lack alpha2delta-1 could make synapses in response to thrombospondin stimulation.

And when the researchers cultured neurons on a plate were at that bioengineering overexpression of receptor neurons synapses products twice in response to stimulation by thrombospondin ummodified than their counterparts.

The new discovery alpha2delta on-1 key in synapse formation has important implications for understanding the causes pain and epilepsy and the development of more effective drugs for these diseases.

We knew alpha2delta-1 is the neuronal receptor for gabapentin, one of the most used drugs in the other world. Gabapentin is often prescribed for chronic pain and epilepsy, and off-label use is widespread in other indications. Until now, the molecular mechanism of action of gabapentin – exactly what it does to prevent seizures or chronic pain – is unknown. But both syndromes involve an excessive number of synaptic connections in the local areas of the brain.

In their new study, Barres and his colleagues found that when gabapentin was administered in mice in the development, limit 1 alpha2delta, thrombospondin prevented from binding to the receptor and in turn prevent synapse. Similarly, blocking thrombosponin, gabapentin was possible to reduce the formation of synapses in vulnerable regions of human brains.

Barres noted that he and his colleagues found that non-existing synapses gabapentin does not dissolve, but only prevents the formation of new ones. This significantly reduces the risk of gabapentin in adults. In the adult human brain, astrocytes THROMBOSPONDIN generally evil and mature neurons do not form many new synapses, although some new synapses form throughout life – for example, in a part of the brain where new memories are established and the injury to neurons places, for example, occur after a stroke.

But new appeal findings raise questions about the effects of gabapentin in situations where synapse formation is widespread and crucial, especially in pregnancies. Most brain synapses are formed during pregnancy and the first months and years after birth. Because gabapentin readily crosses the placenta, which can interfere with the fetus can develop rapidly the brain and the formation of synapses total income quickly.

“It’s a little scary that a drug that can block so powerful synapse is used in pregnant women,” said Barres. “This potential effect on the brain of the fetus should be taken seriously. At this point, doctors believe that gabapentin is the safest anticonvulsant. There is no doubt that pregnant women with epilepsy who are advised by their neurologists to continue their treatment anticonvulsant gabapentin during pregnancy should definitely be on this medication until further notice. But there is no long-term recording is achieved – below gabapentin babies. Our results say that we need to follow these new – born so that their cognitive performance can be studied as they age. “

Leave a Reply

Your email address will not be published. Required fields are marked *