CALCITONIN GENE RELATED PEPTIDE
CRGP (calcitonin gene related peptide) is a molecule that appears to have played an important role in migraine formation since the 1980s. It is involved in the communication between nerve cells and provides the expansion of the vessels (vasodilation) especially in areas where the need for blood increases in the brain. However, this vasodilating feature of CGRP can trigger a headache by causing the body to give an abnormal reaction in migraine patients. In the studies conducted after the learning of this information, the levels of CGRP in the body were measured in migraine patients and healthy individuals without migraine, and this molecule was found to be excessive in the body of migraine patients.
Moreover, headache could indeed be triggered in migraine patients who were given CGRP externally in clinical trials. The culprit was identified and it was time to catch him. Cornering CGRP The first way scientists tried was the simplest. CGRP, which causes migraine, was said, "Let's send a molecule that prevents CGRP from working and prevents it from working, and migraines will end". Although it seems logical and has been shown to be beneficial in many migraine patients, this method was abandoned because important side effects were observed in some patients.
CGRP is an important molecule for the brain to function normally, and it's not something we want to completely neutralize it in the body. Plan B has been launched: disabling CGRP is dangerous, so let's shut down the receptors it needs to act in the brain, and prevent CGRP from triggering its headache, although it can continue to work normally! This idea was put into practice and it was seen that it worked better than the first method and was successful in treatment with less side effects.
CORTICOTROPIN-RELEASING HORMONE
Researchers, who have been trying to overcome stress for years, have made an important step by exploring the center of stress in the brain. According to the information announced at the medical congress held in Bristol earlier this month, the starting point of the stress reaction is located in the '' hypothalamus '', which is a walnut-sized area inside the brain. The nerve cells in this region release the hormone ‘corticotropin '(Crh) in an undesirable situation. This hormone also causes the secretion of another hormone called 'adrenocorticotrope' (ACHT). This hormone flows into the adrenal glands, mixed with blood. The adrenal glands start producing hormones of adrenaline and cortisol, and fat cells begin to spray sugar. The heart rate is accelerating, blood pressure rises to provide energy transfer to the muscles. In such cases, one cannot find opportunities for sex or digestion. However, after the danger passes, the body brakes, cortisol produced with adrenaline returns to its center in the brain. The alarm condition is ending.
The problem starts when the energy that emerges in the stress seizure cannot find an outlet that can act as a valve. Nerve cells can be damaged and dangers such as heart attacks and epileptic seizures may occur. Scientists now state that, thanks to these findings, stress can be overcome more comfortably with hormonal-stabilizing treatments.
Chain reaction in the body
During an stressful event, the hypothalamus releases the CRH hormone. CRH stimulates the pituitary gland to form the hormone ACTH. This reaches the adrenal glands through the bloodstream. The produced adrenaline and cortisol also activate the subcutaneous glands (thymus), defense cells in the spleen and bone marrow. Then cortisol brakes the reaction at the starting point.
UROCORTIN
The most important factor that enables an individual to meet a stranger is the fear reaction that occurs in the brain as a result of the mystery and uncertainty before meeting. Urocortin and similar chemicals formed during fear put the brain circuits under stress. In order to eliminate this tension and stress, we meet the person in front of us. Urocortin is also anorexigenic agent.
CRGP (calcitonin gene related peptide) is a molecule that appears to have played an important role in migraine formation since the 1980s. It is involved in the communication between nerve cells and provides the expansion of the vessels (vasodilation) especially in areas where the need for blood increases in the brain. However, this vasodilating feature of CGRP can trigger a headache by causing the body to give an abnormal reaction in migraine patients. In the studies conducted after the learning of this information, the levels of CGRP in the body were measured in migraine patients and healthy individuals without migraine, and this molecule was found to be excessive in the body of migraine patients.
Moreover, headache could indeed be triggered in migraine patients who were given CGRP externally in clinical trials. The culprit was identified and it was time to catch him. Cornering CGRP The first way scientists tried was the simplest. CGRP, which causes migraine, was said, "Let's send a molecule that prevents CGRP from working and prevents it from working, and migraines will end". Although it seems logical and has been shown to be beneficial in many migraine patients, this method was abandoned because important side effects were observed in some patients.
CGRP is an important molecule for the brain to function normally, and it's not something we want to completely neutralize it in the body. Plan B has been launched: disabling CGRP is dangerous, so let's shut down the receptors it needs to act in the brain, and prevent CGRP from triggering its headache, although it can continue to work normally! This idea was put into practice and it was seen that it worked better than the first method and was successful in treatment with less side effects.
CORTICOTROPIN-RELEASING HORMONE
Researchers, who have been trying to overcome stress for years, have made an important step by exploring the center of stress in the brain. According to the information announced at the medical congress held in Bristol earlier this month, the starting point of the stress reaction is located in the '' hypothalamus '', which is a walnut-sized area inside the brain. The nerve cells in this region release the hormone ‘corticotropin '(Crh) in an undesirable situation. This hormone also causes the secretion of another hormone called 'adrenocorticotrope' (ACHT). This hormone flows into the adrenal glands, mixed with blood. The adrenal glands start producing hormones of adrenaline and cortisol, and fat cells begin to spray sugar. The heart rate is accelerating, blood pressure rises to provide energy transfer to the muscles. In such cases, one cannot find opportunities for sex or digestion. However, after the danger passes, the body brakes, cortisol produced with adrenaline returns to its center in the brain. The alarm condition is ending.
The problem starts when the energy that emerges in the stress seizure cannot find an outlet that can act as a valve. Nerve cells can be damaged and dangers such as heart attacks and epileptic seizures may occur. Scientists now state that, thanks to these findings, stress can be overcome more comfortably with hormonal-stabilizing treatments.
Chain reaction in the body
During an stressful event, the hypothalamus releases the CRH hormone. CRH stimulates the pituitary gland to form the hormone ACTH. This reaches the adrenal glands through the bloodstream. The produced adrenaline and cortisol also activate the subcutaneous glands (thymus), defense cells in the spleen and bone marrow. Then cortisol brakes the reaction at the starting point.
UROCORTIN
The most important factor that enables an individual to meet a stranger is the fear reaction that occurs in the brain as a result of the mystery and uncertainty before meeting. Urocortin and similar chemicals formed during fear put the brain circuits under stress. In order to eliminate this tension and stress, we meet the person in front of us. Urocortin is also anorexigenic agent.
