Protein defect leads to autism behavior star-news.press/wp

summary: A new study reveals that autistic symptoms of mice appear when nerve proteins-MDGA2 and BDNF-fall from balance. MDGA2 usually maintains BDNF/TKB signals in the choice, but when MDGA2 levels decrease, growing neurons and social weaknesses occur.

Mice with a decrease in MDGA2 showed autism -like behaviors, including repeated grooming and social withdrawal. Treatment with peptide that simulates MDGA2 balance restoration and relief symptoms, indicating a possible pathway for future autism treatments.

Main facts:

• Protein defect: Low MDGA2 disrupts BDNF/TKB signals, which leads to ASD -like symptoms.
• Behavioral changes: The affected mice showed frequent behaviors and social deficit.
• Therapeutic capabilities: MDGA2 imitation reduce symptoms, indicating new treatment methods.

source: Plos

In mice, the symptoms of autism arise when a specific pair of nerve proteins is launched from balance, according to a study published on April 1.^street In the open access magazine Biology Plos Written by DongDong Zhao from Wenzhou Medical University, China, Yun-Lu Zhang from Xiamen University, China, and his colleagues.

Nearly 1 % of the world’s population is considered to suffer from autism spectrum disorder (ASD), and shows a series of social and cognitive symptoms. Previous research has linked some ASD genetic factors, including many associated with neurons, but still is not clear exactly how these factors are related.

In this study, Zhao and Zhang and its colleagues used mice to examine the activity of neurons suspected of linking to ASD.

MDGA2 is a protein involved in the transmission of nerve signals, and some mutations in MDGA2 The gene was identified in ASD patients. Experimental experiments revealed that mice with low levels of MDGA2 showed ASD -like symptoms, including repeated grooming and changing social behavior.

These mice also showed an increased activity in some nerve clamps and increasing levels of BDNF, another neurotransmitter that was linked to ASD and works by linking and activating TKB protein. When these mice were treated with artificial peptide that mimic MDGA2 and prevent BDNF/TKB activity, symptoms decreased.

Based on these results along with previous research, the authors indicate that MDGA2 and BDNF maintains a natural balance by competing with each other for TKB protein connection sites, and the disruption of this system can lead to organizational changes in ASD neurons.

This protein system may be a promising target for future therapeutic treatments, but further investigation of the accurate functions of this system and its relationship to ASD symptoms.

“The mutations are in MDGA2 The gene causes autism spectrum disorders (ASD) but the basic mechanism is far.

“Our study reveals a new role for MDGA2 in maintaining BDNF/TKB signals in the Gulf for normal exclusive activity, and shows that MDGA2 deficiency leads to the activation of BDNF/TKB abnormal and high nervous activity, which leads to ASD phenotypes in mice.”

Finance: This work was supported by grants from the National Corporation for Natural Sciences in China (82001442 to DZ, 82130039 and U21A20361 to Y The financiers had no role in designing the study, collecting and analyzing data, publishing, or preparing the manuscript.

On these news, genetics and autism research

author: Claire Turner
source: Plos
communication: Claire Turner – Plus
image: The image is attributed to news of neuroscience

The original search: Open access.
“MDGA2 The deficiency leads to anomalous activation of the BDNF/TKB signal that lies behind the interlocking and autistic changes of autism in miceWritten by Yoon Wu Chang and others. Biology Plos

a summary

MDGA2 The deficiency leads to anomalous activation of the BDNF/TKB signal that lies behind the interlocking and autistic changes of autism in mice

The field of MEMPRIN/A5/MU (MAM), which contains glycosel phosphatidylositol 2 (MDGA2), is a sexy interlocking inhibitor and its mutations are associated with ASD.

However, the detailed physiological function of the MDGA2 and the mechanism behind the MDGA2 obtained by ASD that ASD has not been clarified yet.

Here, we only confirm that MDGA2^+/− Mice show an increase in the transmission of exciting clamp and ASD behaviors, but also determine the activation of neurological signal signals from the brain/tyrosin Kinaz B (BDNF/TKB) in these mice.

We explain that MDGA2 interacts with TKB through the MEMPRIN/A5/MU field, thus competing to connect BDNF to TKB. Both MDGA2 loss and MDGA2 V930i balancing associated ASD enhance BDNF/TKB signals.

More importantly, we make it clear that the inhibition of BDNF/TKB signals by both the small molecular compound and the derivative peptide from MDGA2 can reduce the increase of amino-amino-3-heydroxy-5-methyl-4-vixazole (ampa) MDGICACACACATIC MDGA2-DISCICINCE (MDGA2-DIS-DIS-DIS-DIS-DIS-DISSINC.

These results shed light on a new mechanism that depends on MDGA2-BDNF/TKB which is behind the organization of the interlocking function, which may become a therapeutic target for ASD.