This new drug can help in the end of the trauma disorder to abandon the shock

In a new discovery, scientists at the Basic Science Institute (IBS) and the University of Ewha Womans discovered a new mechanism for security disorders (IBS).

Leaded by Dr. C. Justin Lee at the Center for Perception, Cognition, Suggestions and Professor Liu in Keon at the Iowha University Women, the team showed that excessive Gaba (gamma aminopotrich acid) is produced by stellar cells, which are a star -shaped support cells in the brain, provoking the brain’s ability to get out of the memories of fear. This deficit is an essential feature of post -traumatic necessities and helps explain the reason for the continued painful memories after a long period of the threat.

It is important, the researchers found that a drug is launched in the brain called KDS2010, which blocks an enzyme of monochromatic oxidase responsible for the unnatural GABA production, can reflect symptoms similar to PTSD. The drug has already passed safety experiences in the first stage in humans, making it a strong candidate for future trauma disorder treatments.

It is still difficult to treat post -traumatic disorder, with current drugs that target serotonin paths that provide limited comfort to many patients. The new study focused on the medial frontal lobe (MPFC), which is a decisive brain area to regulate fear, and found that patients with post -traumatic disorder have unusually high levels of GABA and reduce cerebral blood flow in this region. These results appeared from brain imaging studies for more than 380 participants. More importantly, GABA levels have decreased in patients who showed a clinical improvement, pointing to the main role of the chemical in healing.

To detect the origin of this excess GABA, researchers examined the human brain tissue after death and used mouse models that resemble PTSD. They discovered that stellar cells, not neurons, were producing abnormal quantities of GABA through the mono -Emin’s oxidase (MAOB). This star neurological activity derived from stellar cells, which prevents the brain’s ability to forget painful memories.

When the researchers managed KDS2010, a very selective MAOB inhibitor that could be reflected in the Irritable Bowel Syndrome, mice showed natural brain activity and managed to extinguish fear responses. The drug lowering GABA levels, the recovery blood flow in MPFC, and the mechanisms of re -enabled memory extinction. Thus, the study confirms that MAOB is as a major motor for post -traumatic disorder symptoms, and mab in supply as a viable therapeutic path.

The main challenge of the study was to link clinical results in humans with cellular mechanisms in the laboratory. The researchers addressed this by implementing a “reverse” strategy: they started to wipe the clinical brain and move back to determine the cell source of a functional defect, then they confirmed the mechanism and the effects of drugs tested in animal models. This approach led to a new understanding of how the glial cells – which are believed to be negative – are active symptoms.

“This study is the first to determine GABA, which is derived from the stellar cells as a major patient driver for extinction inability to fear in post -traumatic disorder,” said Dr. Won Wajin, a post -PhD researcher and author of the first study. “The results we have reached not only reveal a new mechanism based on the survival under the trauma disorder, but also provides pre -clinical evidence on a new therapeutic approach using MABIB inhibitor.”

Director Justin Lee, who led the study, stressed that “this work represents a successful example of reverse research, as clinical results in man led to discovering the basic mechanisms in animal models. By identifying the star GABA as a satisfactory share such as PTSSIC, there can also be no other reverse share, PTSARSIC cannot also be obtained.

Researchers are planning to continue the investigation of the targeted target treatments for various psychological nervous disorders. With the presence of KDS2010 currently in clinical trials for the second stage, this discovery may soon lead to new options for patients whose symptoms have not responded to traditional treatments.