Will crime really inheritance?"Violence" or genetic prediction!

Readers who have watched Spielberg's classic science fiction movie "Minority Report" must have a deep memory of the "criminal prediction" settings.

However, can "crime" really predict in reality?

"Criminal prediction" may be too science fiction, "violence" may really predict!

Recently, the team of Professor Shi Yun, the Institute of Model of the School of Medicine of Nanjing University, published the latest research papers entitled "Dysfunction of AMPA Receptor Glua3 IS Association Behavior In Human" in Nature's sub -issue "Molecular Psychiatry". The researchers directly proved that the GRIA3 gene was related to the attack behavior of the GRIA3 gene from the SNP of the crowd SNP, revealing the new genetic factors of human attack behavior and helping to solve the development of psychiatric drugs in violence.

For most animals, attack behavior is a positive biological behavior. It can help animals gain a favorable dominance in the population and facilitate resources, territory and reproduction.

However, for humans, attack behavior not only has biological significance, but also has certain social significance. Inappropriate attacks can cause serious damage to society, such as violent crimes. Therefore, research attack behavior has very important biology and sociological significance.

The development of optical genetic tools and neural anatomy allows researchers to summarize the neural circuit behind the attack behavior from the mouse model. The development of large -scale sequencing technology allows researchers to detect genes related to human attack behavior from a genetic perspective. Among them, the inner frontal premiocytic lesions (MPFC) lesions have already caused human impulse and attack behavior. The GRIA3 genes of glutamic acid receptor GLUA3 are related to the attack behavior of human and mice. But still lacks direct evidence to prove the role of the GRIA3 gene.

Fig.1 Mutations in Glua3 Serve as a Marker for Patients with Aggressive Outburssts.

In this study, four European patients with emergencies carry two rare GRIA3 mutants in their bodies, so they show strong attack behavior. The GRIA3 gene mutation of three patients caused the GLUA3 glutamic acid receptor to change the amino acid residue of G630R, and the genetic mutation of another patient caused changes in E787G. By comparing with GRIA3 gene knockout mice models, researchers have determined the direct relationship between GRIA3's dysfunction and attack behavior.

Fig.2 glua3 variants disrupt Ion channel function.

Immediately afterwards, these mutant analysis was performed. Researchers carried clones and transfected to 293T cells on multiple GLUA3 mutants, but the results showed that the G630R mutation was a functional loss of functional mutations (LOF). The function analysis of E787G mutations shows similar results. In order to analyze the cause of these functions, the researchers also showed that the lack of function was due to the destruction of the ion channel instead of the lack of surface transport protein through WesternBlot detection.

Fig.3 The SnP RS3216834 Regulaters GRIA3 Gene Expression.

The aforementioned research shows that Glua3 LOF mutations may be related to human attack behavior. Further, researchers have explored whether genetic factors can affect GLUA3 expression. Therefore, the researchers analyzed the single nucleotide polypentine site (SNP) in the crowd GRIA3 gene seat. The results show that among the 192 high -frequency SNPs, RS3216834 has a single -chain DNA structure (mostly 78%in the crowd (about 78%) with nine birddides (9g) due With 7G, 8G, 10G, and 11G), the transcription of MRNA blocked, further experiments show that 10G and 11G will seriously suppress the expression of GLUA3.

In order to further determine evidence related to the RS3216834 and attack behavior. The researchers conducted an SNP test on 294 male violent criminal prisoners, and found that 9 of them carried RS3216834-10G, and 1 person carried 11G (3.4%). Only two of the 937 normal investigators carried 10G (0.2%). These results again prove that RS3216834 is related to attack behavior.

Fig.4 Behavioral Analysis of GRIA3Y/-Mice

Finally, researchers used GLUA3 to knock out mice to explore the lack of GLUA3 functional neural circuit mechanisms that caused aggressive behavior. After the genetic knockout, the neural activity of the frontal premiral cortex of the mouse decreased. After compensating the GLUA3 in the forehead cortex, the mouse's attack behavior was significantly relieved. These results indicate that the abnormal nerve activity of the prefrontal cortex is a key neural circuit mechanism for aggressive behavior. In summary, this article directly proves that the dysfunction caused by the GRIA3 mutation can cause the attack behavior caused by the GRIA3 mutation. The main mechanism that happened.

The "protagonist" glutamic acid receptor (GRIA3) in this article is considered one of the best candidate genes related to aggression. However, glutamic acid is the main exciting neurotransmitter receptor in the mammalian brain, which is activated during various normal neurophysiology. From this perspective, we can also understand why the mutation of GRIA3 can lead to the occurrence of human violence, which may be due to excessive excitement of the nervous system.

Perhaps, one day, through the detection of GRIA3 mutations, we can prevent and targeted the violent attack -type mental illness.

references:

1.peng, sx.et al. DysFunction of AMPA Receptor Glua3 is associated with aggressive behavior in Human. Mol psychiatry.

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