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We have always believed that gene mutations are the main driving factors of behavioral symptoms related to neurological diseases in brain development.
Our research mainly focuses on how these genes affect the functional activities of key brain regions in brain development and how they are regulated Related molecular signaling pathways, and even how they affect specific neural circuits.
As the field of intestinal microbiota has entered a stage of rapid development in recent years, it is increasingly believed that the function of intestinal microbiota in regulating brain functions is no less than that of genes.
Genes can regulate intestinal microbes, and the latter can regulate the behavioral symptoms of neurological diseases through the intestinal-brain axis.
Therefore, it is reasonable to believe that intestinal flora may be a key mediator in neurodevelopmental diseases caused by gene mutations.
On March 4, 2021, the Mauro Costa-Mattioli research team at Baylor College of Medicine in Houston published an article in Cell, revealing that gut microbiota and genetic mutations interact in neurodevelopmental disorders to mediate complex behavioral disorders.
Contact protein-related protein 2 (CNTNAP2) is a cell adhesion molecule widely distributed in the central and peripheral nervous systems.
It assists in the correct positioning and aggregation of voltage-gated potassium channels on myelinated axons, maintaining and stabilizing resting potentials and actions Potential.
CNTNAP2 knockout mice from different sources.
Researchers found that the mice after CNTNAP2 knockout (CNTNAP2-I mice) showed autistic-like social disorders and were overactive.
The omics analysis of the intestinal flora of these knockout mice found that the diversity of the intestinal flora increased.
After CNTNAP2-I mice and wild-type mice were co-bred in an environment, the pre-existing autism-like behavior disappeared.
This suggests that the intestinal flora may play a key role in it.
Littermates strain CNTNAP2 knockout realizes cross-generational genetic social disorder.
Interestingly, CNTNAP2 knockout mice (CNTNAP2 -L mice, which are derived from CNTNAP2 heterozygotes, are called WT-L mice from the same litter).
) Did not show autism-like behavior disorder, but there was still hyperactivity, and the intestinal flora was no different from wild-type mice.
What's more surprising is that the CNTNAP2 mice, the offspring of CNTNAP2 -L mice mated with CNTNAP2 -L mice, can show autistic behavior disorder and realize intergenerational inheritance.
Germ-free mice received gut microbiota transplantation from CNTNAP2 knockout mice from different sources.
Previous studies have shown that mice raised in a sterile environment exhibit social disorders.
Therefore, the researchers transplanted the intestinal flora of WT-L mice, CNTNAP2-L mice and CNTNAP2-I mice into sterile mice, and found that transplanting wild-type mouse intestinal flora can treat sterility.
The social disorder of mice, the intestinal flora of CNTNAP2-L mice, but not CNTNAP2-I mice, can reverse the social behavior disorder of sterile mice.
These results indicate that CNTNAP2-I mice lack at least one gut flora that is essential for social behavior.
Lactobacillus reuteri (Lactobacillus reuteri) is a lactic acid bacteria that has been reported to occur almost naturally in the intestines of all vertebrates and mammals.
Studies have shown that transplantation of Lactobacillus reuteri can promote the levels of oxytocin in the plasma and paraventricular nucleus of the hypothalamus in mouse models of autism, and reverse social behavior disorders.
The researchers found that the level of Lactobacillus reuteri was reduced in CNTNAP2-I mice.
Then they transplanted the bacteria into CNTNAP2-I mice to significantly improve social disorders.
In addition, they can also repair the ventral tegmental area ( VTA, closely related to social behavior, is also a synaptic plasticity disorder in the downstream brain area of oxytocinergic neurons in the paraventricular nucleus of the hypothalamus. In order to further clarify that Lactobacillus reuteri improves social disorders in CNTNAP2-I mice, the researchers used intestinal flora metabolomics sequencing technology to find that the metabonomic characteristics of KO-I mice and the metabolism of WT-I mice The omics characteristics are obviously different, but the transplantation of Lactobacillus reuteri group did not change this difference.
However, the metabolic signal changes of dihydrobiopterin (BH2) and tetrahydrobiopterin (BH4) are the most significant in the above two types of mice.
BH4 belongs to the coenzyme of aromatic amino acid hydroxylase.
It is the three isoenzymes of nitric oxide synthase (NOS)-endothelial nitric oxide synthase (eNOS), neuronal nitric oxide synthase (nNOS) and inducer Cofactor for type nitric oxide synthase (iiNOS).
The level of BH4 metabolites in CNTNAP2-I mice decreased, and the Lactobacillus reuteri group could promote the increase of its metabolite levels.
In addition, administering BH4 alone can also reverse the social disorder in CNTNAP2-I mice and the synaptic plasticity disorder in the VTA brain area.
In general, this article reveals the different behavioral disorders in neurodevelopmental disorders in which the gut microbiota and gene mutations regulate different behaviors: CNTNAP2-I gene mutations are mainly responsible for overactive symptoms, while gut microbiota is mainly responsible for social disturbances.
This mechanism of gene-intestinal flora interaction is essential for understanding the complex behavioral symptoms of the nervous system.
[References] 1.
https://doi.
org/10.
1016/j.
cell.
2021.
02.
009 The pictures in the article are all from the references
We have always believed that gene mutations are the main driving factors of behavioral symptoms related to neurological diseases in brain development.
Our research mainly focuses on how these genes affect the functional activities of key brain regions in brain development and how they are regulated Related molecular signaling pathways, and even how they affect specific neural circuits.
As the field of intestinal microbiota has entered a stage of rapid development in recent years, it is increasingly believed that the function of intestinal microbiota in regulating brain functions is no less than that of genes.
Genes can regulate intestinal microbes, and the latter can regulate the behavioral symptoms of neurological diseases through the intestinal-brain axis.
Therefore, it is reasonable to believe that intestinal flora may be a key mediator in neurodevelopmental diseases caused by gene mutations.
On March 4, 2021, the Mauro Costa-Mattioli research team at Baylor College of Medicine in Houston published an article in Cell, revealing that gut microbiota and genetic mutations interact in neurodevelopmental disorders to mediate complex behavioral disorders.
Contact protein-related protein 2 (CNTNAP2) is a cell adhesion molecule widely distributed in the central and peripheral nervous systems.
It assists in the correct positioning and aggregation of voltage-gated potassium channels on myelinated axons, maintaining and stabilizing resting potentials and actions Potential.
CNTNAP2 knockout mice from different sources.
Researchers found that the mice after CNTNAP2 knockout (CNTNAP2-I mice) showed autistic-like social disorders and were overactive.
The omics analysis of the intestinal flora of these knockout mice found that the diversity of the intestinal flora increased.
After CNTNAP2-I mice and wild-type mice were co-bred in an environment, the pre-existing autism-like behavior disappeared.
This suggests that the intestinal flora may play a key role in it.
Littermates strain CNTNAP2 knockout realizes cross-generational genetic social disorder.
Interestingly, CNTNAP2 knockout mice (CNTNAP2 -L mice, which are derived from CNTNAP2 heterozygotes, are called WT-L mice from the same litter).
) Did not show autism-like behavior disorder, but there was still hyperactivity, and the intestinal flora was no different from wild-type mice.
What's more surprising is that the CNTNAP2 mice, the offspring of CNTNAP2 -L mice mated with CNTNAP2 -L mice, can show autistic behavior disorder and realize intergenerational inheritance.
Germ-free mice received gut microbiota transplantation from CNTNAP2 knockout mice from different sources.
Previous studies have shown that mice raised in a sterile environment exhibit social disorders.
Therefore, the researchers transplanted the intestinal flora of WT-L mice, CNTNAP2-L mice and CNTNAP2-I mice into sterile mice, and found that transplanting wild-type mouse intestinal flora can treat sterility.
The social disorder of mice, the intestinal flora of CNTNAP2-L mice, but not CNTNAP2-I mice, can reverse the social behavior disorder of sterile mice.
These results indicate that CNTNAP2-I mice lack at least one gut flora that is essential for social behavior.
Lactobacillus reuteri (Lactobacillus reuteri) is a lactic acid bacteria that has been reported to occur almost naturally in the intestines of all vertebrates and mammals.
Studies have shown that transplantation of Lactobacillus reuteri can promote the levels of oxytocin in the plasma and paraventricular nucleus of the hypothalamus in mouse models of autism, and reverse social behavior disorders.
The researchers found that the level of Lactobacillus reuteri was reduced in CNTNAP2-I mice.
Then they transplanted the bacteria into CNTNAP2-I mice to significantly improve social disorders.
In addition, they can also repair the ventral tegmental area ( VTA, closely related to social behavior, is also a synaptic plasticity disorder in the downstream brain area of oxytocinergic neurons in the paraventricular nucleus of the hypothalamus. In order to further clarify that Lactobacillus reuteri improves social disorders in CNTNAP2-I mice, the researchers used intestinal flora metabolomics sequencing technology to find that the metabonomic characteristics of KO-I mice and the metabolism of WT-I mice The omics characteristics are obviously different, but the transplantation of Lactobacillus reuteri group did not change this difference.
However, the metabolic signal changes of dihydrobiopterin (BH2) and tetrahydrobiopterin (BH4) are the most significant in the above two types of mice.
BH4 belongs to the coenzyme of aromatic amino acid hydroxylase.
It is the three isoenzymes of nitric oxide synthase (NOS)-endothelial nitric oxide synthase (eNOS), neuronal nitric oxide synthase (nNOS) and inducer Cofactor for type nitric oxide synthase (iiNOS).
The level of BH4 metabolites in CNTNAP2-I mice decreased, and the Lactobacillus reuteri group could promote the increase of its metabolite levels.
In addition, administering BH4 alone can also reverse the social disorder in CNTNAP2-I mice and the synaptic plasticity disorder in the VTA brain area.
In general, this article reveals the different behavioral disorders in neurodevelopmental disorders in which the gut microbiota and gene mutations regulate different behaviors: CNTNAP2-I gene mutations are mainly responsible for overactive symptoms, while gut microbiota is mainly responsible for social disturbances.
This mechanism of gene-intestinal flora interaction is essential for understanding the complex behavioral symptoms of the nervous system.
[References] 1.
https://doi.
org/10.
1016/j.
cell.
2021.
02.
009 The pictures in the article are all from the references
