A drug developed by Teva according to research at the Technion will make it possible to delay the destruction of nerve cells in Parkinson's patients * Amphetamines and ectasia cause the death of nerve cells in a similar way, and their use will cause Parkinson-like phenomena, says Prof. John Feinberg from the Technion School of Medicine. * Special to the science website
Avi Blizovsky
A drug developed by Teva based on research conducted at the Faculty of Medicine at the Technion may delay the development of the symptoms associated with Parkinson's disease. This is what Prof. John Feinberg from the Rappaport Faculty of Medicine at the Technion says in a special interview for the Hidan website.
"Pharmacology is the science of drugs," explains Prof. Finberg. "My role here at the faculty is research and teaching in basic pharmacology - which mainly discusses the mechanisms of action of drugs. As part of my work, I collaborated with Prof. Mousa Zaim from the same department. Prof. Zaim brought a number of chemical compounds in order to test their action as inhibitors of an enzyme called monoamine oxidase MAO.
It is an enzyme that breaks down neurotransmitters of the type of adrenaline, noadrenaline (a similar substance that is used as a chemical mediator in the body's sympathetic system that guards the heart and blood vessels and prepares the body for action) and dopamine - a relative of the other two, it is also a neurotransmitter in its own right that is especially important in the neurons of the brain."
"The neurons in which dopamine is a chemical mediator are found in the nerve cells that are important for controlling movement and also in the process of determining normal behavior. An excess of dopamine is associated with schizophrenia, and an underactivity of dopamine in the brain is associated with Parkinson's disease."
"In Parkinson's disease, the neurons that use dopamine as a neurotransmitter degenerate and die. The problem with the disease is that you don't see any functional change until the patient has already lost more than 50% of these important dopamine-secreting neurons. We call them dopaminergic, and then we first see signs of Parkinson's disease, which include tremors, Muscle stiffness and difficulty resuming movement, for example a person sitting in a chair, unable to get up.
Is it possible to simply give the body dopamine instead of the substance it does not produce?
Prof. Finberg: "We cannot give dopamine, but instead we give a substance called DOPA, a famous historical substance in this disease, as in the movie AWAKENING, which told about the first discovery in which they found it. At the beginning of the disease, this substance restores the body to the function it lacks. The drug we We found that it inhibits the enzyme monamine acosodate, or rather one of its types, which is responsible for breaking down dopamine in the brain in a normal state. We monitor the enzyme MAO B And the inhibition of this enzyme reduces the breakdown of dopamine and prolongs the stay of dopamine in its receptors and thus restores movement to the body. This drug is developed in cooperation with the Teva company, which passed the drug through all stages of a clinical trial. including experiments in healthy people to understand how the body tolerates the drug and then tests in patients who suffer from Parkinson's disease. The drug is given either alone or together with Dupa. The drug is now approved for use in Europe and, of course, in Israel. It is a drug that improves the quality of life of Parkinson's patients. It has the ability to protect neurons from programmed cell death. DEATH or APOPTOSIS."
"The first clinical trials show that perhaps the drug really inhibits the development of the disease and not only treats the symptoms of the disease. It is also found in models of Parkinson's disease in laboratory animals, mainly in mice and rats that treatment with risagiline protects against toxins that selectively poison the dopaminergic neurons. In my laboratory we breed Innate rat neurons and also see in the plate that rasagiline protects against mortality neuronal."
"My part in the development was in clarifying the preclinical pharmacology of the patient. It was important for us to know that it was possible to give joint treatment between risgiline and dopa without unwanted effects on the heart, blood vessels and animal behavior. And showing that risgiline selectively inhibits the MAO B enzyme was important To show that it does not inhibit the second form of MAO A because then we could not give it together with dopa. Also the initial work on the effect of risgiline to prevent death cells (neuroprotection) - works in animals."
Dopamine and stimulant drugs
"As part of Brain Days, my lecture was about dopamine and the brain. Since this is a school, I usually talk about substances like ecstasy and amphetamine (speed, in jargon) AMPHETAMINE," says Dr. Finberg. According to him, since this is a lecture that will be given in schools, he requests To clarify how these drugs work on the brain, and what damage they cause, regardless of the question of addiction associated with them.
"These drugs are called stimulants because they accelerate behavior. Ecstasy is known as a popular substance among youth among those who turn to drugs, these substances cause their effects due to the release of dopamine in the brain. This effect can be harmful to neurons because although dopamine in normal amounts is processed and eliminated by the body, but when Released in large quantities as by these drugs, it can cause a toxic effect on neurons."
The concern is that, as I explained before, a Parkinson's patient can lose 50% of their neurons before you see anything clinical. It is possible to cause damage to these neurons without seeing a clear effect, but the results can be expressed several years later, so it is especially important to explain to the youth to protect their brains and not to use stimulant drugs such as ecstasy and amphetamines. They are also addictive and of course there are addictive drugs that are also dangerous. The problem is that the use of ecstasy is not a typical use for addiction. Because addiction is compulsive use. Today we see a lot of drug use like ecstasy not intensively but casually, still it can be harmful to the brain. After the neurons die, nowadays there is not much to do. A few years ago a group of people in California injected an illegally synthesized drug into a bone and by mistake a substance was created that poisoned all the dopaminergic neurons and caused irreversible Parkinson's disease for everyone. Some of them are even in their twenties. It was a famous case, the substance involved was called MPTP. This shows the danger of using prohibited substances that are sometimes contaminated, since there is no regulation that determines the chemical quality, it is possible that the preparation is not chemically clean, contamination of the substance itself with side effects of chemical synthesis, unlike in medicines that are prepared with high quality. Whoever buys a drug from a drug dealer has no idea what is inside it."
days of the brain
The Israeli Association for Neuroscience is mobilizing to give lectures to the general public in order to know a little more about what the researchers are doing at the academic ivory tower and also to tell the audience a little more about the functions of the brain, what other diseases there are in the brain, how we try to fight it. The event is held in collaboration with the Beshaar Association, an association of professors that tries to connect the academy with the community in all aspects of the academy.
The Brain Days will be held across the country between March 19 and 24 by the Israeli Association for Neuroscience.
The full list of lectures all over the country, mainly in Pis clusters and community centers
The brain savant
https://www.hayadan.org.il/BuildaGate4/general2/data_card.php?Cat=~~~400385662~~~238&SiteName=hayadan
